Infections Associated With Diabetes
Summary
Evidence from centuries of clinical practice supports the relationship between diabetes and infections. Possible mechanisms include the effect of hyperglycemia on the immune system, increased risk of local tissue ischemia, neuropathy, and the association of diabetes with other comorbidities, such as obesity and heart failure, that independently increase the risk of infection. Individuals with diabetes are more likely to develop certain infections compared to those without diabetes, including urinary tract infections (such as asymptomatic bacteriuria, pyelonephritis, renal and perinephric abscess), respiratory tract infections, sepsis, lower extremity infections, deep subcutaneous tissue infections, and tuberculosis. In addition, several rare but serious infections occur almost exclusively in people with diabetes, including necrotizing otitis externa, rhinocerebral mucormycosis, emphysematous pyelonephritis, and Fournier’s gangrene. Though it remains unclear whether diabetes is associated with a higher risk of acquiring COVID-19, evidence suggests diabetes is associated with significantly elevated risk of severe and fatal complications from the infection.
In the United States in 1999–2023, the age-standardized percentage of deaths with any infection ranged from 2.3% to 16.8% in persons with diabetes compared with 3.5% to 14.6% in persons without diabetes, with respiratory tract infections accounting for the highest percentage of deaths in both groups. In addition, during 1999–2021, the age-standardized percent of hospital discharges listing any infection ranged from 19.5% to 34.9% in persons with diabetes compared with 12.1% to 23.4% in persons without diabetes. Skin and connective tissue infections were the most common for individuals with diabetes, while respiratory tract infections accounted for the highest percentage of hospital discharges in those without diabetes. Individuals with diabetes who develop infections face higher rates of hospital admission, longer stays, and more complications, which in turn increase healthcare costs. This article summarizes the body of evidence on the relationship between diabetes and infectious disease risks and outcomes. It also outlines implementation strategies to facilitate adoption of evidence-based care for diabetes-related infections.
Introduction
The relationship between diabetes and infections, such as erysipelas, pneumonia, and tuberculosis (TB), has been documented in clinical practice for centuries (
) (
,
). Historically, diabetes contributed considerably to morbidity and mortality, particularly prior to the advent of insulin and antibiotics (
,
). Recent studies quantifying the burden of infection-related complications in people with diabetes have shown a significant risk of hospitalization for infections, particularly foot infections, respiratory infections, urinary tract infections (UTIs), sepsis, and postoperative infections (
). Individuals with diabetes who develop infections also face higher rates of hospital admission, longer stays, and more complications, which in turn increase healthcare costs (
). In the post-COVID (coronavirus disease of 2019) pandemic world, it is important to note that although diabetes does not increase the risk of contracting COVID-19, it significantly elevates the risk of severe and fatal complications from the infection (
). In addition, certain rare and sometimes fatal infections, known as signal infections, occur more commonly and are pathognomonic for diabetes, including emphysematous pyelonephritis (EPN), necrotizing otitis externa (NOE), mucormycosis, and Fournier’s gangrene (
).
Summary of Infections Associated With Diabetes
Despite advances in understanding and managing infections in diabetes, large cohort studies show that the risk of hospitalization and death from infections attributable to diabetes remains substantial. A 2024 Swedish population-based study demonstrated significantly higher rates of hospital admissions and mortality among individuals with diabetes compared to those without (
), while global analyses confirmed that infection contributes disproportionately to mortality in type 2 diabetes. Respiratory tract infections, followed by skin and connective tissue infections, remain the most common infections diagnosed in people with diabetes (
,
,
,
). Evidence suggests that diabetes disrupts host-related factors, such as the consolidation and integrity of the mucosa and skin, and targets the immune system at multiple levels, impairing both innate and adaptive immunity by reducing the function of complement, neutrophils, NK cells, and T cells (
). This dysregulation weakens the immune system, making individuals with diabetes more susceptible to severe infections (
).
This article reviews the burden of infectious diseases, mechanisms that increase susceptibility to infections, and strategies for evidence-based care of infections in persons with diabetes; this content updates the Diabetes in America, 3rd edition, chapter Infections Associated With Diabetes (
). The types of infections described in this article are summarized in
.
Data Sources and Limitations
Numerous sources of U.S. data among persons of all ages were analyzed for this article. It is important to recognize that with large, national datasets underreporting and/or misreporting of data can occur. For example, infection-related deaths among individuals with diabetes may not be accurately documented on death certificates when compared to those without diabetes. Similarly, hospital discharge data may not reflect all appropriate diagnoses upon release after inpatient hospitalization. In addition, national data sources often do not reliably differentiate between type 1 and type 2 diabetes, and as a result, all data from persons with diabetes were analyzed as a combined group, which may mask differences in infection risk by diabetes type. Furthermore, in places where the sample size is small, generalizability to all subpopulations may be limited. Despite these limitations, the information available through national datasets using International Classification of Diseases, Ninth or Tenth Revision (ICD-9 or ICD-10) codes (
) to compute infection rates provides important information to understand the relationship between diabetes and infections.
Healthcare Cost and Utilization Project 1999–2021
The Healthcare Cost and Utilization Project (HCUP) is the largest collection of longitudinal hospital care data in the United States. HCUP is a family of healthcare databases developed through a federal-state-industry partnership and sponsored by the Agency for Healthcare Research and Quality (AHRQ). HCUP brings together data from state organizations, hospital associations, private data organizations, and the federal government to create all-payer, encounter-level healthcare data that can be used to investigate a broad range of health policy issues. Infections were identified using ICD-9 and ICD-10 diagnosis codes, as microbiologic and antibiotic prescription data were not uniformly available in the national datasets. Although this coding-based approach aligns with prior national studies, it may lead to misclassification or underestimation of mild infections.
National Ambulatory Medical Care Surveys 1999–2022
The National Ambulatory Medical Care Survey (NAMCS) is a national survey designed to meet the need for objective, reliable information about the provision and use of ambulatory medical care services in the United States. Findings are based on a sample of visits to nonfederal, employed, office-based physicians who are primarily engaged in direct patient care. Infections were identified using ICD-9 and ICD-10 diagnosis codes.
National Vital Statistics System 1999–2023
The National Vital Statistics System (NVSS) is the oldest and most successful example of intergovernmental data sharing in public health. The National Center for Health Statistics (NCHS) collects and disseminates the official vital statistics of the United States. These data are provided through contracts between NCHS and vital registration systems operated in the various jurisdictions legally responsible for the registration of vital events—births, deaths, marriages, divorces, and fetal deaths.
Overview of Infections in Individuals With Diabetes
In the NVSS 1999–2023, the age-standardized percentage of deaths attributed to any infection ranged from 2.3% to 16.8% among persons with diabetes and 3.5% to 14.6% among persons without diabetes. Respiratory tract infections accounted for the largest proportion of infection-related deaths in both groups, with a pronounced increase observed in 2020–2022 during the COVID-19 pandemic (
,
).
Percentage of Deaths Caused by Infection, by Diabetes Status and Infection Type, U.S., 1999–2023. Diabetes status and infections are defined by International Classification of Diseases, Ninth and Tenth Revision codes (Appendix Table A1). HIV,
Based on data from the HCUP 1999–2021, the age-standardized percentage of hospital discharges listing any infection ranged from 19.5% to 34.9% in persons with diabetes and 12.1% to 23.4% in persons without diabetes (
,
,
,
,
, and
,
). Before the COVID-19 pandemic, skin and soft tissue infections (SSTIs) were the most frequently listed infections in hospital discharge records for individuals with diabetes, followed by respiratory tract infections. During and after the pandemic, however, respiratory tract infections became the most commonly listed infections in people with diabetes. In contrast, respiratory tract infections consistently represented the largest proportion of infections documented in hospital discharge records among those without diabetes. The sharp increase in UTIs listed in hospital discharge records for individuals with diabetes beginning in 2016 (from 1.7% to 9.8%) is most likely attributable to the transition from ICD-9 to ICD-10 coding in late 2015, which introduced more detailed categories for UTIs and led to more consistent documentation in discharge data, rather than reflecting a sudden epidemiologic surge.
Age-Standardized Percentage of Hospital Discharges Listing Infection, by Diabetes Status and Infection Type, U.S., 1999–2021. Diabetes status and infections are defined by International Classification of Diseases, Ninth and Tenth Revision codes
Age-Standardized Percentage of Hospital Discharges Listing Any Infection, by Diabetes Status, U.S., 1999–2021. Diabetes status and infections are defined by International Classification of Diseases, Ninth and Tenth Revision codes (Appendix Table A1).
Age-Standardized Percentage of Hospital Discharges Listing Respiratory Tract Infections, by Diabetes Status, U.S., 1999–2021. Diabetes status and respiratory tract infections are defined by International Classification of Diseases, Ninth and Tenth
Age-Standardized Percentage of Hospital Discharges Listing Urinary Tract Infections, by Diabetes Status, U.S., 1999–2021. Diabetes status and urinary tract infections are defined by International Classification of Diseases, Ninth and Tenth Revision
Age-Standardized Percentage of Hospital Discharges Listing Skin and Connective Tissue Infections, by Diabetes Status, U.S., 1999–2021. Diabetes status and skin and connective tissue infections are defined by International Classification of Diseases,
Age-Standardized Percentage of Hospital Discharges Listing Hospital-Acquired Infections, by Diabetes Status, U.S., 1999–2021. Diabetes status and hospital-acquired infections are defined by International Classification of Diseases, Ninth and Tenth
Based on NAMCS data, physician office visits for infection ranged from 1.0% to 5.1% in persons with diabetes compared with 2.5% to 3.7% in persons without diabetes over the time period 1999–2019 (
,
). Data on community health center visits in 1999–2022 among persons with or without diabetes are also provided in
.
Age-Standardized Percentage of Outpatient Visits to a Physician Pertaining to Infections, by Diabetes Status, U.S., 1999–2019. Diabetes status and infections are defined by International Classification of Diseases, Ninth and Tenth Revision codes
General Infections in Individuals With Diabetes
Respiratory Tract Infections
Influenza and Pneumonia
Individuals with diabetes (type 1, type 2, or gestational) are at high risk for complications, hospitalization, and death from influenza (
,
,
). The Centers for Disease Control and Prevention (CDC) estimates that 30% of adults hospitalized with influenza in the United States in recent seasons had diabetes (
). Observational studies also indicate an increased incidence of influenza in individuals with diabetes (
,
,
). An analysis of HCUP 1999–2021 data showed a higher percentage of hospital discharges listing influenza as a diagnosis in individuals with diabetes compared to individuals without diabetes in recent years (
,
). An analysis using data from the National Health and Nutrition Examination Surveys (NHANES) 1999–2010 showed that individuals with diabetes had a 3.6-fold increased risk of influenza- and pneumonia-specific morbidity after adjusting for comorbidities (
).
Age-Standardized Percentage of Hospital Discharges Listing Influenza, by Diabetes Status, U.S., 1999–2021. Diabetes status and influenza are defined by International Classification of Diseases, Ninth and Tenth Revision codes (Appendix Table A1).
The typical incubation period for influenza is one to four days. Common signs and symptoms include an abrupt onset of fever, malaise, myalgia, and a nonproductive cough. Molecular assays, such as nucleic acid amplification tests, are preferred for diagnosis due to their high sensitivity and specificity (
). Multiplex reverse transcriptase polymerase chain reactions (RT-PCR) can detect multiple pathogens simultaneously and should be used when both influenza and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; the virus associated with COVID-19) are circulating or when coinfection is suspected.
Individuals with diabetes face significantly worse outcomes from influenza, including higher rates of hospitalization for influenza or pneumonia, increased intensive care unit (ICU) admission, and elevated risk of myocardial infarction following infection (
,
,
). Bacterial co-infection is also frequent, with Staphylococcus aureus and Streptococcus pneumoniae being the most frequent pathogens reported (
,
). However, studies comparing the microbiological differences in bacterial co-infections between patients with and without diabetes are lacking, and further research is needed to better characterize these differences.
Prophylactic influenza vaccination reduces hospital admissions and mortality related to influenza in individuals with diabetes (
). The Advisory Committee on Immunization Practices (ACIP) recommends annual influenza vaccination for all individuals with diabetes age ≥6 months (
). Although not contraindicated, the ACIP advises caution when administering the live attenuated influenza vaccine (LAIV) to individuals with diabetes (
). This is due to concerns that individuals with chronic medical conditions, including diabetes, may have altered immune responses or increased risk of complications from live vaccines. The inactivated vaccine given by intramuscular injection is used most commonly in adults and is preferred in people with diabetes. Available evidence demonstrates that both the immunogenicity and effectiveness of seasonal influenza vaccines in people with diabetes are comparable to those observed in individuals without diabetes (
).
Antiviral treatment is recommended as soon as possible for any patient diagnosed or suspected of influenza who is at higher risk of complications, including those with diabetes (
). Oral or enteric oseltamivir is the preferred antiviral agent for admitted patients (
).
Other viruses, such as respiratory syncytial virus (RSV) and SARS-CoV-2, can also cause severe disease in people with diabetes (
,
). The ACIP recommends a single RSV vaccine for all adults age ≥75 years and for adults age ≥60 years with risk factors for severe diseases, including individuals with diabetes who have end-organ damage (e.g., diabetic retinopathy, nephropathy, neuropathy, or cardiovascular disease) or requiring treatment with insulin or a sodium-glucose cotransporter-2 (SGLT) inhibitor (
) (
).
Vaccine Recommendations for Patients With Diabetes
While high-quality evidence is limited, existing literature suggests that diabetes is associated with an increased risk of community-acquired pneumonia (CAP). One systematic review and meta-analysis reported a pooled relative risk (RR) of 1.64 (95% confidence interval [CI] 1.55–1.73) of CAP in individuals with diabetes compared to individuals without diabetes; however, all 15 studies included in this analysis had a high risk of bias (
). It remains debatable whether in-hospital mortality in patients admitted with CAP is higher in individuals with diabetes compared to those without diabetes (
).
Individuals with diabetes are at high risk for invasive pneumococcal disease, including pneumococcal bacteremia (with or without pneumonia), meningitis, and other focal invasive infections, such as empyema, septic arthritis, and osteomyelitis. One population-based study found that the incidence of invasive pneumococcal disease in adults age 18–64 years with diabetes was 3.5 times higher (95% CI 3.2–3.9) compared to individuals without diabetes (
). Diabetes is also associated with increased mortality in patients with invasive pneumococcal diseases (hazard ratio [HR] 1.91, 95% CI 1.23–3.03) (
).
Pneumococcal vaccination is recommended for all children, adults age ≥50 years, and adults age ≥19 years with certain immunocompromising conditions, including diabetes (
) (
).
Evidence from randomized trials demonstrates vaccine efficacy in diabetic populations: post-hoc analysis of the CAPiTA trial showed that PCV13 significantly reduced vaccine-type pneumonia hospitalizations in adults with diabetes age ≥65 years (odds ratio [OR] 0.237, 95% CI 0.008–0.704, p=0.002) (
). Observational studies with PPV23 show effectiveness within the first-year post-vaccination (OR 0.63, 95% CI 0.45–0.89 for pneumonia hospitalization), though protection appears to wane thereafter (
).
Important differences in vaccine immune responses exist between diabetic and nondiabetic populations. Studies in type 1 diabetes demonstrate impaired responses to T cell-dependent protein antigens, while responses to pneumococcal polysaccharide antigens (PPV23) remain intact (
,
). For conjugate vaccines, which elicit T cell-dependent responses, antibody levels decline more rapidly in people with type 2 diabetes at 8 months post-vaccination compared to individuals without diabetes (
). In children with type 1 diabetes, protection against pneumococcal colonization from PCV7 vaccination in infancy was not effective after several years, further supporting the need for booster doses to maintain immunity in this population (
). While additional booster immunizations have been shown to overcome impaired vaccine responses to T cell-dependent antigens in type 1 diabetes in controlled studies with other vaccines, clinical data demonstrating that pneumococcal vaccine boosters improve clinical outcomes in populations with diabetes are lacking (
).
Sinusitis and Bronchitis
No direct comparative data are available to determine whether individuals with diabetes are more likely to develop bacterial sinusitis and bronchitis than those without diabetes. While sinusitis and bronchitis are predominantly managed in ambulatory care settings, comparative data from outpatient visits is lacking. Analysis of HCUP data from 1999–2021 shows similar rates of hospital discharges for sinusitis and bronchitis in individuals with and without diabetes (
,
).
Age-Standardized Percentage of Hospital Discharges Listing Sinusitis and Bronchitis, by Diabetes Status, U.S., 1999–2021. Diabetes status and sinusitis and bronchitis are defined by International Classification of Diseases, Ninth and Tenth Revision
COVID-19
Diabetes has been recognized as a risk factor for severe disease since the early days of the COVID-19 pandemic (
,
) (
,
). An early study of 450 people admitted with COVID-19 found that diabetes was associated with greater odds of ICU admission (OR 1.59, 95% CI 1.01–2.52), mechanical ventilation (OR 1.97, 95% CI 1.21–3.20), and death (OR 2.02, 95% CI 1.01–4.03) after adjusting for comorbidities (
). However, the accumulation of natural immunity in the population, emergence of less virulent viral variants, expanded therapeutic options, improvements in COVID-19 management, and increased vaccination rates have since led to a reduction in disease severity across all patients, including those with diabetes. Though it remains unclear whether diabetes is associated with a higher risk of acquiring COVID-19, diabetes is associated with worse outcomes for individuals who contract COVID-19 (
).
Age-Standardized Percentage of Hospital Discharges Listing COVID-19, by Diabetes Status, U.S., 2019–2021. Diabetes status and COVID-19 are defined by International Classification of Diseases, Ninth and Tenth Revision codes (Appendix Table A1).
COVID-19 can precipitate diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state, and severe insulin resistance (a pathophysiological state in which cells fail to respond normally to insulin, requiring higher insulin levels to achieve glucose uptake and maintain normoglycemia), even in patients without a history of diabetes (
). A systematic review reported that hyperglycemia was more strongly associated with in-hospital mortality (adjusted OR 1.28, 95% CI 1.09–1.50) and ICU admission (crude OR 1.82, 95% CI 1.17–2.84) than diabetes (
). Severe insulin resistance has also been observed in critically ill patients with COVID-19, which may improve with the resolution of infection.
Some studies have suggested an increased incidence of diabetes following COVID-19. A meta-analysis of nine studies with nearly 40 million participants found that the relative risk of diabetes after COVID-19 infection was elevated (RR 1.62, 95% CI 1.45–1.80), with increased risk for individuals with both type 1 diabetes (RR 1.48, 95% CI 1.26–1.75) and type 2 diabetes (RR 1.70, 95% CI 1.32–2.19) (
). Another systematic review and meta-analysis of children and adolescents found an increase in type 1 diabetes incidence in the first year of the pandemic compared with the pre-pandemic period (incidence rate ratio [IRR] 1.14, 95% CI 1.08–1.21), with elevated incidence persisting in the second year (IRR 1.27, 95% CI 1.18–1.37) (
). An analysis of U.S. veterans who survived the first 30 days after a COVID-19 diagnosis showed a significant increase in the incidence of diabetes at 6 months (HR 8.23, 95% CI 6.36–9.95) (
). However, a more recent study of U.S. veterans with incident diabetes found that those with SARS-CoV-2 infection had a 22% higher chance of diabetes remission (RR 1.22, 95% CI 1.14–1.29), with this association attenuated among nonhospitalized participants (RR 1.11, 95% CI 1.04–1.20), suggesting that increased surveillance or transient hyperglycemia rather than permanent metabolic dysfunction may explain some COVID-associated diabetes cases (
).
Post-COVID conditions (PCC), also known as postacute sequelae of SARS-CoV-2 (PASC) or long COVID, are chronic conditions that may develop after SARS-CoV-2 infection and persist for at least 3 months. These conditions can present as continuous, relapsing, remitting, or progressive disease affecting one or more organ systems. Some studies suggest that diabetes is a risk factor for PCC, though definitive evidence is lacking (
,
).
Antiviral treatments are recommended for individuals with diabetes diagnosed with COVID-19, particularly if multiple risk factors for severe disease are present. These therapies are most effective when administered early after symptom onset. Ambulatory treatment options include nirmatrelvir/ritonavir, molnupiravir, and remdesivir (
). Steroids are recommended only for patients hospitalized with severe or critical COVID-19 who require supplemental oxygen or ventilatory support.
The ACIP recommends COVID-19 vaccination for all individuals age ≥6 months after shared clinical decision-making with healthcare providers (
). Discussions should emphasize that the risk-benefit of vaccination is highest for those at an increased risk for severe COVID-19, including individuals with diabetes. In the United States, two mRNA vaccines (Moderna COVID-19 vaccine and Pfizer-BioNTech COVID-19 vaccine) and an adjuvanted recombinant protein vaccine (Novavax COVID-19 vaccine) are available (
). Individuals with diabetes, regardless of type or vaccination status, generally show lower antibody responses and immunogenicity to COVID-19 vaccination (
) compared to those without diabetes, though most still achieve seroconversion after full vaccination. Despite lower immunogenicity, COVID-19 vaccines remain effective in reducing severe disease and death in patients with diabetes, though vaccine effectiveness is modestly lower and breakthrough infection may be more frequent in this group (
).
Urinary Tract Infections
Asymptomatic Bacteriuria
Asymptomatic bacteriuria (ASB) is a significant concern in patients with type 2 diabetes, given their heightened vulnerability to infections, particularly those affecting the urinary tract. The Infectious Diseases Society of America (IDSA) defines ASB as the presence of one or more species of bacteria growing in the urine at specified quantitative counts (≥105 colony-forming units [CFU]/mL or ≥108 CFU/L), irrespective of the presence of pyuria, in the absence of signs or symptoms attributable to UTI (
).
Studies of the global prevalence and management of ASB in type 2 diabetes patients have shown regional variations. For example, the prevalence of ASB in patients with type 2 diabetes in rural southwestern Nigeria is 26.1%, with Escherichia coli being the most commonly isolated pathogen (
). In a prospective case control study in India, the prevalence of ASB was significantly higher in both men and women with diabetes compared with controls (17.5% in patients with type 2 diabetes vs. 10% in controls, p=0.015) (
). A meta-analysis of more than 4,000 patients further highlighted the prevalence and risk factors associated with ASB in type 2 diabetes, showing a worldwide prevalence of 23.7% (
).
A number of clinical factors increase the risk of ASB in patients with type 2 diabetes. A meta-analysis demonstrated that patients with ASB were, on average, 3.18 years older than those without ASB (weighted mean difference [WMD] 3.18 years, 95% CI 1.91–4.45, p<0.001), indicating that advancing age is a significant risk factor, likely related to age-associated immune decline and urinary tract changes (
). Similarly, higher glycated hemoglobin (A1C) levels were observed in the ASB group (WMD 0.63%, 95% CI 0.43%–0.84%, p<0.001), reflecting poorer glycemic control and highlighting the role of chronic hyperglycemia in increasing infection susceptibility (
). Longer duration of diabetes was also associated with greater risk (WMD 2.54 years, 95% CI 1.54–5.43, p<0.001), consistent with the cumulative impact of metabolic and vascular complications over time (
). Female sex was a strong independent predictor (OR 1.07, 95% CI 1.02–1.12, p=0.002), aligning with well-established anatomic and microbiologic risk factors (
). Comorbidities and diabetes complications further amplify this vulnerability. Together, these findings underscore the multifactorial nature of ASB risk in people with type 2 diabetes, with age, glycemic control, disease duration, sex, and metabolic factors all contributing to increased susceptibility.
There is no evidence that ASB treatment can reduce the incidence of UTI. The most recent IDSA guidelines recommend that ASB should be screened for and treated only in pregnant women or in individuals prior to undergoing invasive urologic procedures. Treatment is not recommended for healthy women, older women or men, or persons with diabetes, indwelling catheters, or spinal cord injury (
). This recommendation is based on the understanding that treating ASB in these populations does not significantly reduce the risk of developing symptomatic UTI but increases the risk of adverse effects of therapy, including antibiotic resistance.
Despite IDSA guidelines recommending against routine treatment of ASB in patients with diabetes due to an unfavorable risk-benefit profile, emerging evidence continues to highlight its clinical significance. In a prospective cross-sectional study, 400 patients with type 2 diabetes without symptoms of UTI were compared with 200 healthy controls (
). The prevalence of ASB was significantly higher among individuals with type 2 diabetes compared with controls (17.5% vs. 10%) (
). A subset of 64 type 2 diabetes patients with ASB was followed for 6 months; during this period, 21.8% developed symptomatic UTI (
). Independent predictors of progression to infection included postmenopausal status, poor glycemic control, longer duration of diabetes, diabetic nephropathy, and glycosuria (
). Notably, ASB was associated with worsening glycemic control over time, although renal function remained stable during follow-up (
). This study demonstrates that ASB in type 2 diabetes is common, associated with identifiable risk factors, and confers a measurable risk of subsequent symptomatic infection. These findings reinforce the importance of risk stratification and careful clinical monitoring, particularly in high-risk subgroups, while aligning with current guidelines that discourage routine antimicrobial therapy in the absence of symptoms.
The complex interplay between diabetes management and infection risk, particularly in ASB, highlights the importance of early detection, appropriate antibiotic use, and preventive measures to effectively manage these infections in patients with diabetes.
Cystitis and Pyelonephritis
Cystitis and pyelonephritis are common UTIs that present unique challenges for individuals with diabetes due to their increased susceptibility to immune and urinary system changes. Symptoms of cystitis include painful and frequent urination without vaginal discharge or irritation and rarely lead to fever. On the other hand, patients with pyelonephritis typically present with more severe symptoms, such as high fever, chills, and back pain. A urine culture is recommended for diagnosing and managing pyelonephritis and recurrent and complicated UTIs.
A study examining the risk of UTIs in individuals with newly diagnosed type 2 diabetes found that UTI diagnosis was more common in subjects with type 2 diabetes than without type 2 diabetes (9.4% vs. 5.7%, p<0.0001) (
). Recurrence of UTI was also more likely in persons with type 2 diabetes (1.6% vs. 0.6%, p<0.0001). In a logistic regression, individuals with type 2 diabetes had a significantly greater likelihood of developing a UTI during follow-up compared with those without type 2 diabetes (adjusted OR 1.54, 95% CI 1.47–1.60) (
). Insulin use and longer duration of diabetes were also associated with increased risk of UTI (
).
Patients with diabetes, particularly those with type 2 diabetes, are at an increased risk of hospitalization due to pyelonephritis. Studies indicate that women with diabetes are 6–15 times more likely to be hospitalized for acute pyelonephritis (APN) compared to women without diabetes, while men with diabetes have a 3.4–17 times higher hospitalization rate than men without diabetes (
). This elevated risk is due to factors such as impaired immune response and more severe infections in individuals with diabetes. A South Korean study using a Health Insurance Review and Assessment Service claim database found that among patients with APN, 12.4% had diabetes (
). The in-hospital mortality rate was higher in patients with diabetes compared to those without (2.6/1,000 events in the diabetes group vs. 0.3/1,000 in the group without diabetes, p<0.001). After controlling for covariates, diabetes was associated with higher in-hospital mortality in APN patients. The impact of diabetes on in-hospital mortality varied significantly with age, with the effect being most significant for individuals age 15–49 years.
SGLT2 Inhibitors and UTI Risk
SGLT2 inhibitors increase urinary glucose excretion, which may theoretically promote bacterial growth in the urinary tract and raise the risk of UTIs; however, evidence for this association has been mixed to date. A meta-analysis of 77 randomized controlled trials involving more than 50,000 participants found no significant increase in UTI incidence compared with placebo or other agents (RR 1.05, 95% CI 0.98–1.12) (
). Similarly, major cardiovascular and renal outcome trials (CANVAS, CREDENCE, DECLARE–TIMI, EMPA-REG) did not show a significant difference in UTI rates (
). Observational data have shown more variability. A real-world cohort study in Thailand found a higher incidence of UTIs among SGLT2 inhibitor users (33.5%) compared with nonusers (11.7%), with a hazard ratio of 3.70 (95% CI 2.60–5.29) (
). Other registry-based studies suggest no increased risk of severe or complicated UTIs in SGLT2 inhibitor users (
,
). Current evidence supports continued use of SGLT2 inhibitors with appropriate patient counseling and monitoring rather than avoidance due to UTI concerns.
Emphysematous Pyelonephritis in Patients With Diabetes
EPN is a severe and life-threatening necrotizing infection of the renal parenchyma, occurring in people with poorly controlled type 2 diabetes. It is characterized by gas within the kidney tissues and is linked to a high risk of morbidity and mortality (
). Early studies reported an EPN mortality rate as high as 80%; however, data from 2007 found the overall mortality rate has decreased to 25%, ranging from 11% to 42% (
).
The typical clinical presentation of EPN in patients with diabetes includes fever, costovertebral angle tenderness, severe hyperglycemia, and acute kidney injury (AKI) (
). The most common causative organisms are Escherichia coli and Klebsiella pneumoniae, followed by Proteus (
). Risk factors for EPN include longer duration of diabetes, nephropathy, chronic kidney disease (CKD), hypertension, a history of symptomatic UTI in the prior year, renal calculi, and obstruction (
).
Managing EPN in patients with diabetes is challenging due to a lack of consensus on the optimal approach. Patients with diabetes face high complication risks, especially with renal obstruction, worsening azotemia, and recurrent UTIs. These factors, along with poor glycemic control and renal impairment, predict failure in medical management. EPN complications include DKA, hyperosmolar hyperglycemic state, and multiorgan dysfunction (
,
,
). Early, aggressive treatment is essential, especially if septic shock, altered mental status, or renal deterioration occur. Early imaging and a multidisciplinary approach, including antibiotics and surgery, can improve outcomes in patients not responding to standard pyelonephritis therapy (
,
,
).
Renal and Perinephric Abscesses
Renal and perinephric abscesses are localized collections of pus that develop either within the kidney (renal abscess) or in the tissue surrounding the kidney (perinephric abscess). These abscesses typically arise from severe bacterial infections, such as complicated UTIs or as a result of direct extension from infections in adjacent organs. They can also occur due to the spread of bacteria via the bloodstream (hematogenous spread).
Patients with diabetes are at a markedly higher risk of developing renal and perinephric abscesses compared to those without diabetes. Studies of renal and perinephric abscesses reveal that diabetes is associated with a longer hospital stay but does not significantly increase the risk of in-hospital mortality. In a cohort study conducted in Taiwan, patients with diabetes had a longer hospital stay by approximately 3.38 days compared to those without diabetes; however, the mortality rates between the two groups were similar, with 2.3% for patients with diabetes and 3.4% for those without diabetes (
). This finding suggests that while diabetes may not worsen immediate mortality outcomes, it complicates recovery, potentially due to factors like impaired immune function, poorer overall health, and higher rates of complications, such as glycemic instability and infection (
,
). Therefore, managing patients with diabetes and these abscesses requires careful attention to reduce hospital stay through aggressive medical and sometimes surgical interventions.
Skin and Soft Tissue Infections
SSTIs are common in both outpatient and inpatient settings, with patients with diabetes being at higher risk for complications. An analysis of more than 2 million SSTI cases in U.S. health plans (2005–2010) found that 10% occurred in individuals with diabetes, with abscesses/cellulitis being the most common (
). Patients with diabetes had more than five times the complication rate and four times the hospitalization rate compared to those without diabetes. The most frequent complications in hospitalized patients with diabetes included bacteremia and sepsis (
,
). These findings highlight the need for targeted prevention efforts, such as blood sugar control, daily skin hygiene, regular foot care, and immediate treatment of any skin wounds, among individuals with diabetes to reduce morbidity and healthcare costs associated with SSTIs (
).
Age-Standardized Percentage of Hospital Discharges Listing Sepsis, by Diabetes Status, U.S., 1999–2021. Diabetes status and sepsis are defined by International Classification of Diseases, Ninth and Tenth Revision codes (Appendix Table A1). Data
Analysis of HCUP 1999–2021 data found that the average percentage of hospital discharges listing skin and connective tissue infections among individuals with diabetes decreased slightly from a high of 12.2% in 2015 to 10.7% in 2021 (
,
). In individuals without diabetes, the average percentage of hospital discharges listing skin and connective tissue infections was 4.1% in 2021.
Several host-related factors in patients with diabetes predispose them to an increased risk of SSTIs, with hyperglycemia serving as the predominant underlying mechanism. Infection rates and associated complications, including mortality, are notably higher in individuals with type 1 diabetes compared to those with type 2 diabetes, directly correlating with the degree of glycemic control in both diabetes types (
).
Fungal Skin and Soft Tissue Infections
Fungal skin infections are notably more prevalent among individuals with diabetes (
). Diabetes is recognized as a significant risk factor for the development of onychomycosis, as well as oral and vulvovaginal candidiasis (
,
). These infections are clinically relevant due to their high incidence in patients with poorly controlled diabetes (
,
,
).
Age-Standardized Percentage of Hospital Discharges Listing Oral and Vaginal Candidiasis, by Diabetes Status, U.S., 1999–2021. Diabetes status and oral and vaginal candidiasis are defined by International Classification of Diseases, Ninth and Tenth
CandidiasisCandidiasis frequently manifests in patients with diabetes, particularly when glycemic control is inadequate. Oral candidiasis presents with white patches on the tongue, oral mucosa, and throat, while genital candidiasis manifests as pruritus and a burning sensation in the genital area. Diagnosis is typically achieved through clinical examination, microscopic evaluation, and culture techniques (
). The association between diabetes and fungal infections is well established, particularly in the context of urogenital infections like vulvovaginal candidiasis and balanitis, as well as oral candidiasis caused by Candida species. The use of SGLT2 inhibitors has been linked to an increased risk of urogenital colonization by Candida species, predisposing patients to subsequent infection (
).
Urogenital InfectionsVulvovaginal candidiasis is characterized by vulvar soreness and pruritus, often accompanied by a thick, cottage cheese-like vaginal discharge (
). In males with diabetes, Candida spp. can cause balanitis or balanoposthitis, presenting as a pruritic rash with sores, erosions, or papules, often accompanied by subpreputial discharge. The relationship between hyperglycemia and Candida proliferation beneath the prepuce is well documented. Although Candida accounts for less than 20% of all balanoposthitis cases, it remains the most common pathogen in males with diabetes (
). Coinfections with other pathogens, including Streptococcus pyogenes, can complicate the clinical presentation. Treatment of candidal balanitis or balanoposthitis includes topical and oral antifungals, such as clotrimazole or fluconazole. Improving hygiene, keeping the area clean and dry, and avoiding harsh soap or scented products are crucial preventive measures. In severe or recurrent cases, circumcision is recommended to reduce future infection (
).
OnychomycosisOnychomycosis, an infection of the nail plate by dermatophytes, yeasts, and nondermatophytic molds, commonly affects both fingernails and toenails in patients with diabetes. Dermatophytes, particularly Trichophyton rubrum and Epidermophyton floccosum, are the predominant causative agents; other possible causative agents are Trichophyton interdigitale and Trichophyton tonsurans. Microsporum spp. is rarely related to onychomycosis episodes. Onychomycosis is highly prevalent in patients with diabetes, affecting approximately one-third of this population. The infection often begins in interdigital spaces before extending to the nails, contributing to significant morbidity in affected individuals. Oral antifungal therapy (terbinafine, itraconazole, and fluconazole) is the most effective treatment. Liver function tests should be monitored, especially with terbinafine and itraconazole. Topical therapy with antifungal agents (efinaconazole, tavaborole, and ciclopirox) along with debridement can be used in mild or limited infections. Combinations of treatments (topical plus systemic treatment) and nail thinning strategies are required to obtain better results in a short time and avoid relapses (
,
).
Bacterial Skin and Soft Tissue Infection
Poor glycemic control has been linked to an increased risk of bacterial skin and soft tissue infections (
). Complicated SSTIs (cSSTIs) are of particular concern because skin breakdown in patients with advanced diabetes and peripheral arterial disease provides a portal of entry for bacteria. Patients with diabetes are more likely to be hospitalized with cSSTIs and to experience related complications than patients without diabetes (
).
Suaya et al. conducted a retrospective cohort study using U.S. healthcare claims data, examining 2,227,401 episodes of SSTIs among individuals age 0–64 years enrolled in U.S. health plans between 2005 and 2010 (
). The study found that 10% of these infections occurred in individuals with diabetes. Abscesses and cellulitis were the most common types of infection in individuals with and without diabetes, accounting for 66% and 59% of cases, respectively (p<0.01). Complication rates for SSTIs, including osteomyelitis, gangrene, sepsis, limb amputation, and necrotizing fasciitis (NF), were more than five times higher in individuals with diabetes compared to those without (4.9% vs. 0.8%, p<0.01) in ambulatory settings, and hospitalization rates were also significantly higher among patients with diabetes (4.9% vs. 1.1%, p<0.01). Additionally, 75.6% of SSTIs among patients with diabetes occurred in the 45–64-years age group compared to 31.1% among individuals without diabetes in the same age group (p<0.01) (
).
Of all skin and connective tissue infections, cellulitis and impetigo were the most frequent hospital discharge diagnoses among individuals with diabetes in the United States in 1999–2021 (
,
). In superficial ulcerations and cellulitis, Streptococcus species and Staphylococcus aureus (both methicillin-susceptible and methicillin-resistant) are the most common causative bacteria in patients with diabetes. Corynebacterium species may play an important role in biofilm formation and can cause infection known as erythrasma, presenting as shiny, hyperpigmented patches in areas of increased maceration and friction; erythrasma occurs more frequently in individuals with diabetes and obesity (
). Prompt diagnosis, glycemic management, antibiotic therapy, and in some cases, timely surgical debridement are needed to improve outcomes for superficial SSTIs.
Age-Standardized Percentage of Hospital Discharges Listing Cellulitis and Impetigo, by Diabetes Status, U.S., 1999–2021. Diabetes status and cellulitis and impetigo are defined by International Classification of Diseases, Ninth and Tenth Revision
Diabetic Foot Ulcers and Osteomyelitis
Diabetic foot ulcers arise from a complex interplay of factors, including peripheral neuropathy, peripheral arterial disease, foot deformities, and infections. Foot infections are common and can result in severe consequences. Infected diabetic foot ulcers can be differentiated from noninfected ones by the presence of purulent discharge along with erythema, warmth, and tenderness around the ulcer. More than half of all foot ulcers become infected, making infection the most frequent precursor to lower extremity amputation. The microbial complications associated with these infections can range from superficial cellulitis to chronic osteomyelitis and gangrene requiring amputation. Previously, coverage for polymicrobial infection was recommended for diabetic foot infections; however, current recommendations are that antibiotic therapy is unnecessary for wounds without confirmed soft tissue or bone infections. Mild infections warrant empiric treatment targeting gram-positive cocci, whereas moderate to severe infections, often due to drug-resistant pathogens, may require cultures or biopsies to establish a diagnosis and necessitate the use of broad-spectrum antimicrobials that are effective against aggressive gram-negative aerobes and obligate anaerobes (
).
Diabetic foot infections represent the most common cause of diabetes-related hospitalizations and lower extremity amputations. In cases of acute diabetic foot infection, there is often a delay in identifying the causative pathogen, necessitating the use of empirical antibiotic therapy. The lifetime risk of developing a foot ulcer in patients with diabetes is estimated at approximately 34%, and more than 50% of these ulcers become infected during their course (
).
Foot infections should be clinically diagnosed based on the presence of inflammation or purulence and then categorized according to severity. This classification aids clinicians in determining the appropriate course of action, such as hospitalization, imaging studies, or surgical intervention. Diabetic foot infections can be caused by a variety of pathogens, either individually or in combination, with gram-positive cocci, particularly staphylococci, being the most prevalent. To improve outcomes and prevent amputations, a systematic approach to the management of diabetic foot infections is essential. Without prompt and appropriate treatment, diabetic foot infections can become refractory to therapy or progress to septic gangrene. Among the various classification systems for diabetic foot ulcers, the IDSA/International Working Group on the Diabetic Foot (IWGDF) system is recommended for categorizing infections (
) (
,
).
Classification of Diabetic Foot Infections
Since all skin wounds naturally contain microorganisms, their presence alone—even of virulent species—does not necessarily indicate an infection. Therefore, diagnosing a diabetic foot infection must be based on clinical evaluation, with wound cultures used to identify the causative organisms and assess their antibiotic sensitivities (
). Age-standardized hospital discharge data from the HCUP 1999–2021 demonstrate that approximately 4.4% of patients with diabetes had foot ulcers listed on their discharge summaries compared with 0.7% of patients without diabetes (
,
).
Age-Standardized Percentage of Hospital Discharges Listing Foot Ulcers, by Diabetes Status, U.S., 1999–2021. Diabetes status and foot ulcers are defined by International Classification of Diseases, Ninth and Tenth Revision codes (Appendix Table A1).
Osteomyelitis should be suspected in patients with deep, chronic, nonhealing ulcers or exposed bone. In the evaluation of an infected open wound, a probe-to-bone test is recommended. According to the IWGDF guidelines, the diagnostic approach to diabetic foot osteomyelitis should be guided by the patient’s pretest probability (
). In patients with a low likelihood of osteomyelitis, a negative probe-to-bone test effectively excludes the diagnosis, whereas a positive result in high-risk patients strongly supports it (strong recommendation; high-quality evidence). Markedly elevated inflammatory markers, particularly the erythrocyte sedimentation rate, may further suggest osteomyelitis when clinical suspicion exists (weak recommendation; moderate-quality evidence). A definitive diagnosis generally requires histopathologic confirmation and, ideally, microbiological culture of an aseptically obtained bone specimen. This is indicated when the diagnosis remains uncertain or when antibiotic susceptibility data are essential (strong recommendation; moderate-quality evidence). When bone biopsy is not feasible, a probable diagnosis can be established through a combination of findings from the probe-to-bone test, serum inflammatory markers, plain radiography, magnetic resonance imaging (MRI), or radionuclide imaging (strong recommendation, low-quality evidence). Soft tissue or sinus tract cultures should not be used to guide antibiotic therapy, as they do not reliably reflect bone pathogens (strong recommendation, moderate-quality evidence). Plain radiographs are recommended for all cases of nonsuperficial diabetic foot infection (strong recommendation, low-quality evidence). When advanced imaging is warranted, MRI remains the preferred modality; if unavailable or contraindicated, alternative options include white blood cell-labeled radionuclide scintigraphy, single-photon emission computed tomography/computed tomography (SPECT/CT), or fluorine-1-fluorodeoxyglucose positron emission tomography (FDG-PET) (weak recommendation, moderate-quality evidence (
).
In the HCUP 1999–2021, the percentage of hospital discharges listing osteomyelitis in patients diagnosed with diabetes was 1.0% in 2021, after peaking at 1.7% in 2014 and 2015, compared to 0.1% for patients without diabetes (
,
).
Age-Standardized Percentage of Hospital Discharges Listing Osteomyelitis, by Diabetes Status, U.S., 1999–2021. Diabetes status and osteomyelitis are defined by International Classification of Diseases, Ninth and Tenth Revision codes (Appendix
An interdisciplinary team, including an infectious disease specialist, a vascular or general surgeon or a podiatrist trained in the management of diabetic foot ulcers, and an endocrinologist, is essential for the optimal management of foot ulcers in individuals with diabetes. Initial empiric antimicrobial therapy, adjusted to pathogen-specific treatment once culture results are available, along with surgical debridement and offloading are appropriate strategies depending on the severity of the condition. In severe cases, such as an unsalvageable foot, untreatable infection, or critically ischemic limb, minor amputation performed in a timely manner may prevent future requirements of major amputations.
Deep Subcutaneous Tissue Infections
The incidence of NF in the United States is estimated to range from 500 to 1,500 cases annually; however, this figure may be underestimated due to the challenges in diagnosing NF accurately (
,
). NF and Fournier’s gangrene are notably more common among individuals with diabetes, with up to 75% of NF cases occurring in patients with diabetes (
). Analysis of the National Surgical Quality Improvement Database from 2005 to 2008 revealed that 45% of patients with necrotizing soft tissue infections had diabetes. Despite this association, diabetes was not identified as a risk factor for mortality in the same database during the same period (
).
NF often presents with nonspecific superficial signs, such as erythema and edema, making early diagnosis challenging. It is crucial for clinicians to promptly differentiate between cellulitis, which can be managed with antimicrobial therapy, and NF, which necessitates urgent surgical intervention. Delayed treatment of NF can lead to catastrophic outcomes, including limb amputation, organ failure, and a significantly elevated risk of mortality.
Both NF and cellulitis are marked by skin erythema, edema, and warmth, with fever occasionally present. However, patients with cellulitis typically remain hemodynamically stable, whereas those with NF may exhibit extreme tenderness or pain and can rapidly progress to hemodynamic instability and tissue necrosis. Elevated levels of creatine kinase or aspartate aminotransferase may also indicate a deep tissue infection in NF.
Differentiating between cellulitis and NF is particularly challenging due to the often-vague initial presentation of NF. Diagnostic accuracy may be further compromised by factors such as the use of nonsteroidal anti-inflammatory drugs, which can mask key symptoms, including fever, and the severe, disproportionate pain characteristic of NF. Additionally, patients with diabetic neuropathy may not experience the expected level of pain, complicating the clinical assessment further (
).
NF is classified into two main types: polymicrobial (Type I) and monomicrobial (Type II). Type I, the most common form, involves both aerobic and anaerobic bacteria and is prevalent in older adults with chronic conditions. Type II is typically caused by gram-positive bacteria like group A Streptococcus (GAS) and methicillin-resistant Staphylococcus aureus (MRSA), often leading to severe clinical outcomes, such as toxic shock syndrome. While Type I is associated with chronic disease, Type II can occur in individuals without obvious risk factors. Other less common but more virulent pathogens, including Pseudomonas and Vibrio vulnificus, have led to suggestions of a third classification type, although this is not universally accepted. Additionally, NF can be categorized by infection site, with specific forms like Ludwig angina and Fournier’s gangrene, though these distinctions are more relevant for epidemiological purposes than immediate clinical management (
).
Fournier’s gangrene is a specific type of NF that affects the external genitalia and perianal region. It is characterized by thrombosis of the supplying arteries, resulting in gangrene of the skin and subcutaneous tissue. This condition is often associated with severe systemic toxicity and can lead to multiple organ failure (
). A retrospective study conducted by Taken et al. included 65 patients admitted to the emergency surgical unit with Fournier’s gangrene between January 2006 and August 2014. The study analyzed the anatomical sites of gangrene, predisposing factors, etiological factors, and patient outcomes and found that 29 out of the 65 patients (44.6%) had diabetes (
). Necrotizing infections involving muscles, such as clostridial myonecrosis and non-clostridial myonecrosis, have also been described in individuals with diabetes; however, it is not clear whether these infections occur more frequently in individuals with diabetes compared with the general population.
Analysis of HCUP 1999–2021 data showed that approximately 0.8% of patients with diabetes were discharged with Fournier’s gangrene as a diagnosis (
,
). In contrast, only 0.1%–0.2% of those without diabetes had Fournier’s gangrene listed as a diagnosis at hospital discharge. Post-marketing surveillance has raised concerns that SGLT inhibitors may be associated with an increased risk of Fournier’s gangrene. Owing to the rarity of this condition, clinical trial data are insufficient to establish a definitive relationship. Consequently, real-world observational studies are needed to better evaluate the potential association between SGLT2 inhibitor use and Fournier’s gangrene in individuals with type 2 diabetes (
).
Age-Standardized Percentage of Hospital Discharges Listing Fournier’s Gangrene, by Diabetes Status, U.S., 1999–2021. Diabetes status and Fournier’s gangrene are defined by International Classification of Diseases, Ninth and Tenth
Hospital-Acquired Infections
Hyperglycemia impairs immune function, creating an ideal environment for the growth of bacterial pathogens (
). Among individuals with diabetes, acute illness often exacerbates glycemic control, leading to inpatient hyperglycemia, which is associated with a higher risk of hospital-acquired infections (HAIs), prolonged hospital stays, and increased in-hospital mortality (
,
,
).
An analysis of HCUP 1999–2021 data showed that individuals with diabetes have a higher rate of HAIs (
,
), including sepsis and postoperative wound infections. While HAIs increased in both groups, individuals with diabetes consistently had higher infection rates, peaking around 2015 before decreasing slightly and then stabilizing. Conversely, despite higher infection rates, mortality associated with HAIs was consistently lower in individuals with diabetes (
,
). The reason for higher mortality in patients without diabetes is unclear.
Mortality Among Patients With Hospital-Acquired Infections, by Diabetes Status, U.S., 1999–2023. Diabetes status and hospital-acquired infections are defined by International Classification of Diseases, Ninth and Tenth Revision codes (Appendix Table
Diabetes is a well-recognized risk factor for postoperative wound infections (
,
). In a systematic review and meta-analysis of 94 studies, diabetes was independently associated with increased surgical site infection risk (OR 1.53, 95% predictive interval 1.11–2.12), with a stronger effect observed in cardiac surgery (OR 2.03) (
). Diabetes also increased the risk of infections following abdominal, podiatric, and head and neck surgeries (
,
,
). However, there is conflicting literature regarding the risk of infection following orthopedic procedures (
,
,
). Optimal perioperative glycemic targets have not been established. A systematic review and meta-analysis found that intensive glycemic control during surgery did not reduce all-cause mortality (RR 1.08, 95% CI 0.88–1.33) or infectious complications (RR 0.75, 95% CI 0.55–1.04) compared to conventional glycemic control; however, intensive glycemic control significantly increased the risk of hypoglycemia (RR 3.36, 95% CI 1.69–6.67) (
).
Age-Standardized Percentage of Hospital Discharges Listing Postoperative Wound Infections, by Diabetes Status, U.S., 1999–2021. Diabetes status and postoperative wound infections are defined by International Classification of Diseases, Ninth and
Diabetes is also a major risk factor for catheter-related bloodstream infections (CRBSI). A meta-analysis revealed that individuals with diabetes admitted to the ICU had three times the odds of developing CRBSI (OR 3.06, 95% CI 2.56–3.66) (
). Similarly, diabetes increases the risk of CRBSI in hemodialysis patients (OR 2.52, 95% CI 1.95–3.25) (
). These findings highlight the need for heightened vigilance and preventive measures for individuals with diabetes who have central venous catheters during hospital admissions.
Diabetes is a recognized risk factor for invasive candidiasis in hospitalized patients. Invasive candidiasis refers to systemic Candida infections that can affect the bloodstream, deep tissues, and organs, representing a severe and potentially life-threatening complication (
). A study of nonneutropenic patients admitted to Internal Medicine wards showed that diabetes increased the risk of invasive candidiasis in hospitalized patients by sevenfold (OR 7.31, 95% CI 3.91–13.61) (
). In critically ill patients, a systematic review and meta-analysis demonstrated that diabetes remained independently associated with invasive candidiasis after adjusting for confounding variables, with a pooled adjusted odds ratio of 3.7 (95% CI 2.24–6.1) (
). Invasive candidiasis is associated with high mortality rates, and early recognition and treatment are essential for improving outcomes (
).
Although it remains unclear whether diabetes is a direct risk factor for Clostridioides difficile colonization, diabetes is associated with an increased risk of fulminant C. difficile infection (CDI) following cardiac surgery (OR 1.74, 95% CI 1.15–2.63) (
). Additionally, a meta-analysis identified diabetes as a risk factor for community-acquired CDI (OR 1.15, 95% CI 1.05–1.27) (
), although diabetes does not appear to be associated with higher mortality in CDI (
,
).
Careful management of inpatient hyperglycemia may help reduce the incidence of HAIs. In a cluster randomized trial, four surgical and four medical wards were randomized to receive either usual care or early intervention for hyperglycemia. In the early-intervention wards, patients with hyperglycemia and diabetes were identified within 24 hours of admission and managed by a specialist team, including a diabetologist, endocrinology fellow, and diabetes nurse. The team provided individualized treatment, prescribing subcutaneous insulin and glucose-lowering medications to achieve safe glycemic control while avoiding hyper- or hypoglycemia. By the end of the trial, HAIs were significantly lower in the intervention group (adjusted OR 0.20, 95% CI 0.07–0.58) (
).
Periodontal Disease
Managing periodontal complications is crucial for improving overall health outcomes in patients with diabetes. Periodontal disease, or gum disease, refers to infections and inflammation of the structures surrounding the teeth, primarily caused by bacterial plaque buildup. It begins with gingivitis, characterized by inflamed, red, and bleeding gums. If untreated, it can progress to periodontitis, where the infection damages deeper tissues, including the bone, potentially leading to tooth loss. Various risk factors like smoking, genetics, and systemic diseases, such as diabetes, exacerbate the severity of periodontal disease.
The prevalence of periodontal disease is significantly higher in patients with diabetes compared to the general population. Individuals with diabetes are three to four times more likely to develop periodontal disease, with higher risks in smokers and those with uncontrolled diabetes (
). A study in North India found that 95.1% of the 427 participants had some degree of periodontal destruction, with severe periodontitis more common among those with poor oral hygiene and poor glycemic control (
). Various factors affect the prevalence of periodontal disease in patients with diabetes. Annual dental visits, being female, and having a college education are associated with a lower risk, while smoking, older age, non-White race, and lower-income are associated with significantly increased risk (
).
Periodontal disease has been associated with tooth loss and reported as more prevalent among people with diabetes than among those without diabetes. The overall prevalence of tooth removal in a study that included 155,280 people was 38.3%. People with diabetes had a significantly higher prevalence of tooth removal. Respondents with diabetes were 1.46 times as likely (95% CI 1.30–1.64) to have at least one tooth removed compared with respondents without diabetes (
).
Other Infections Associated With Diabetes
Necrotizing (Malignant) Otitis Externa
NOE is a potentially life-threatening infection of the temporal bone. It was previously known as “malignant otitis externa,” but this terminology was changed to avoid patient misinterpretation and anxiety. The incidence of NOE appears to be rising, potentially due to increasing antibiotic resistance, a growing population of individuals with diabetes, an aging demographic, and heightened clinical awareness of the condition (
). Pseudomonas aeruginosa is the most common causative agent, followed by others including MRSA, Proteus mirabilis, Klebsiella spp., Aspergillus fumigatus, various other gram-negative bacteria, and fungi. Pseudomonas and MRSA are associated with longer hospitalization and increased complications. NOE primarily affects older adults, individuals with diabetes, and/or immunocompromised patients. Advancing age is associated with increased mortality, while African Americans have been found to have higher rates of comorbidities (
,
,
,
).
NOE presents with symptoms like otalgia, otorrhea, presence of granulation tissue, aural fullness, and hearing loss. Facial nerve palsy is a concerning sign associated with higher mortality. A study analyzing 786 NOE cases found a mean hospital length of stay of 18.6 days, with a 9.3% ICU admission rate (
).
Diagnosis of NOE is based on presence of risk factors for immunosuppression (which increases susceptibility), characteristic clinical signs and symptoms along with their duration, and diagnostic studies, including serum inflammatory markers, microbiology studies and imaging modalities, such as CT, MRI, and PET 2‐deoxy‐2‐[fluorine‐18] fluoro‐D‐glucose with CT (18F‐FDG‐PET/CT). 18F-FDG-PET/CT scans are highly sensitive and specific for detecting, localizing, and confirming resolution of NOE compared to other imaging modalities but are limited by their availability and the need for specialized interpretation. Biopsies are helpful in cases unresponsive to empiric antibiotics (
). Timely and accurate diagnosis, combined with appropriate antibiotic therapy, surgical intervention when indicated, and optimization of glycemic control are considered essential to improving outcomes in NOE, although direct evidence linking glycemic control to reduced mortality remains limited (
).
Rhinocerebral Mucormycosis
Mucormycosis is a severe invasive fungal infection caused by the fungi mucormycetes (previously known as zygomycetes) belonging to the order Mucorales, with the main genera being Rhizopus, Rhizomucor, Liechtheimia, or Mucor (
). These infections are usually spread through inhalation of spores, absorption of infected meals, or inoculation of injured or damaged tissue (
). The incidence of mucormycosis is rising in several countries due to an increasing at-risk population, improved awareness, and the development of novel diagnostic methods. Two large nationwide prospective surveillance studies conducted in France and Greece identified diabetes as a significant underlying host-related factor for the development of mucormycosis, contributing to 7.5% (41/550 cases) and 15.9% (17/107 cases) of cases, respectively (
,
). The majority of the cases were attributed to hematopoietic malignancies (358/550 cases, 65.1%) followed by trauma (44/550 cases, 8.0%). COVID-19 has emerged as one of the newer and significant risk factors for mucormycosis, along with diabetes (
). Mucormycosis was recently added to the World Health Organization (WHO) fungal priority pathogens list as “high priority” concern (
,
,
).
Mucormycosis is classified by the anatomical region affected, including pulmonary, rhinocerebral, cutaneo-articular, orbital, and disseminated forms. Rhinocerebral mucormycosis is the most common type in patients with diabetes, accounting for 46.4% of cases (19 of 41), particularly in those with DKA (
,
,
). Initially the disease may present with a broad spectrum of manifestations, and hence, one proposed algorithm suggests looking for certain red flag signs in patients with diabetes, including sinus pain, cranial nerve palsy, diplopia, proptosis, periorbital swelling, orbital apex syndrome, or palatine ulcer (
). Black eschar, although pathognomonic, may not be present in all cases.
Given the consistently high mortality rate associated with this infection, maintaining a high level of clinical suspicion is crucial for timely diagnosis and aggressive treatment. To reduce mortality, proactive treatment with antifungal medications like amphotericin B and aggressive surgical debridement with direct tissue sampling are essential (
,
). Additionally, stringent glycemic control and management of DKA are necessary, as both have been shown to significantly impact survival outcomes in patients with rhinocerebral mucormycosis (
,
). The workup requires a multidisciplinary approach, incorporating laboratory markers of inflammation and imaging studies, such as CT, MRI, and FDG-PET, to identify the infected zone and plan surgical boundaries.
Emphysematous Cholecystitis
Emphysematous cholecystitis (EC) is a rare but life-threatening form of acute cholecystitis, characterized by the presence of gas within the gallbladder wall or lumen. This condition, most commonly caused by gas-forming bacteria such as Clostridium perfringens, Escherichia coli, and Bacteroides fragilis, can progress to gangrenous cholecystitis and peritonitis, carrying high morbidity and mortality rates (
). New analyses of hospital discharge listings from the HCUP 1999–2021 demonstrated similar percentages of EC-related discharges (0.1%–0.2%) for those with and without diabetes; thus, diabetes was present in approximately 50% of EC cases, underscoring its role as a key risk factor (
,
). These data support a previous report also showing that 50% of patients diagnosed with EC have diabetes (
). This proportion is attributed to ischemic environments, particularly in individuals with diabetic microangiopathy, which reduce tissue perfusion and impair phagocyte mobility, thereby weakening the immune response and facilitating gas-forming bacterial growth (
).
Age-Standardized Percentage of Hospital Discharges Listing Emphysematous Cholecystitis, by Diabetes Status, U.S., 1999–2021. Diabetes status and emphysematous cholecystitis are defined by International Classification of Diseases, Ninth and Tenth
The initial presenting signs of EC include right upper quadrant pain, fever, jaundice, nausea, and vomiting, making it challenging to distinguish from gallstone-associated cholecystitis and cholangitis based on signs and symptoms alone (
). Crepitus on abdominal palpation is a pathognomonic sign, though rarely present. Diagnosis is based on radiographic findings, with a CT scan (preferred) or X-ray revealing a gaseous halo around the gallbladder and a gas-fluid level within the gallbladder (
,
). Ultrasound is less preferred due to its low sensitivity and high operator dependency. Additionally, laboratory investigations—such as inflammatory markers, liver enzymes, and blood and fluid cultures—are crucial for confirming the diagnosis, identifying specific microbes, and tailoring antibiotic treatments accordingly. Treatment involves conservative measures such as broad-spectrum antibiotics, intravenous fluids, and surgical interventions, such as laparoscopic or open cholecystectomy or percutaneous cholecystostomy, depending on the clinical presentation and patient stability.
Group B Streptococcus Infections
Group B Streptococcus (GBS), or Streptococcus agalactiae, is a gram-positive coccus characterized by a polysaccharide capsule that contains the cell wall-specific Lancefield Group B antigen (
). GBS is an opportunistic bacterium normally found in healthy adults as part of their genitourinary and gastrointestinal flora. In a large systematic review and meta-analysis, the prevalence of GSB was found to be 25% and 20% for rectal and vaginal swabs, respectively (
). Among U.S. adults, the overall incidence of GBS infection has risen from 1.50 per 100,000 population during 1975–1990 to 2.73 in 1991–2005 and further to 3.79 in 2006–2018 (
). Additionally, the incidence increases with age, reaching 9.13 per 100,000 population in adults age ≥50 years and 19.40 per 100,000 population in those age ≥65 years. Between 2008 and 2016, a significant increase was observed in the percentage of patients with GBS infection who had diabetes, rising from 43.5% to 53.4% (
).
GBS has several serotypes. From 2008 to 2016, the prevalence of serotypes Ib, II, and IV increased, while serotypes Ia, III, and V became less common (
). In North America, serotype V was the most common, accounting for 43.48% of isolates from nonpregnant adults. The frequency of serotype Ib doubled, serotype II increased by more than 70%, and serotype IV quadrupled, contributing significantly to the overall rise in infections. Additionally, serotype III was more prevalent in Europe and Asia, while serotype VI was notably present in Asia but rare elsewhere (
,
,
). These shifts in serotype distribution highlight the evolving landscape of GBS infections, particularly in populations with diabetes, underscoring the need for ongoing surveillance and targeted interventions.
GBS can cause invasive disease in neonates, pregnant women, nonpregnant adults with comorbidities, and older adults. In a systematic review and meta-analysis, diabetes was identified as the primary underlying comorbid condition, present in 15%–64% of invasive GBS (iGBS) cases in nonpregnant adults (
). This was followed by cancer and malignancies, and to a lesser extent, cardiovascular disease, hypertension, cirrhosis, kidney disease, obesity, and chronic obstructive pulmonary disease (COPD) (
). Among U.S. adults in 2008–2016, iGBS most commonly manifested as SSTI (34.0%), bacteremia without a focus (32.3%), osteomyelitis (13.3%), pneumonia (10.2%), and septic arthritis (10.2%) (
). Rarely, iGBS presented as intra-abdominal infection (3.1%), endocarditis (2.1%), meningitis (1.15%), or NF (0.5%) (
). Diabetes was associated with iGBS presenting more frequently as SSTIs (
). Fortunately, the case fatality ratio of iGBS has progressively decreased over time, from 15.12%–15.9% during 1975–1989 to 8.8%–11.83% in 1990–2004, and further down to 7.91%–9.9% in 2005–2021 (
,
,
).
Diagnosis of GBS infections requires high clinical suspicion in combination with diagnostic studies, including laboratory investigations and imaging studies, depending on the signs and symptoms with which the patient is presenting. Blood, fluid, and tissue cultures are helpful in identifying the pathogen and the antimicrobial susceptibility to tailor antibiotics and aid in faster recovery. This is important especially as the antimicrobial resistance among GBS isolates has increased over time, with significant resistance observed to tetracycline (up to 95%), erythromycin (up to 54.8%), and clindamycin (up to 43.2%). While most isolates remained susceptible to penicillin, some resistance was noted in a few studies. Additionally, resistance to levofloxacin, linezolid, and vancomycin was rare but present (
,
), highlighting the need for ongoing surveillance and targeted interventions, especially in populations with diabetes.
Diabetes and Tuberculosis
The link between diabetes and TB is well established, with TB remaining one of the leading causes of death in low- and middle-income countries (
,
). Despite numerous public health efforts to address diabetes, its prevalence continues to rise at an alarming rate. This increase is occurring more rapidly in low- and middle-income countries—regions already heavily impacted by infectious diseases—compared to high-income countries. As of 2021, more than 10.5% of the global adult population, equivalent to 536.6 million individuals, were living with diabetes. This figure is projected to increase to 12.2%, or 783.2 million adults, by 2045 (
). In 2023, the WHO estimated 10.8 million (95% uncertainty interval [UI] 10.1–11.7 million) people fell ill with TB worldwide, of whom 6 million were men, 3.6 million were women, and 1.25 million were children (
). Of these TB patients, 95% live in developing countries, which are also home to 79% of the global population of adults with diabetes (
,
).
Most evidence regarding diabetes as a risk factor for TB comes from case-control studies conducted worldwide. Al-Rifai et al. conducted a meta-analysis of 44 studies, encompassing a total of 58,468,404 individuals from 16 countries, to evaluate the association between diabetes and the risk of active TB (
). The analysis revealed that individuals with diabetes had a 3.59-fold (95% CI 2.25–5.73), 1.55-fold (95% CI 1.39–1.72), and 2.09-fold (95% CI 1.71–2.55) increased risk of active TB in prospective, retrospective, and case-control studies, respectively. The association was influenced by factors such as country income level (3.16-fold in low/middle-income vs. 1.73-fold in high-income countries), background TB incidence (2.05-fold in countries with >50 vs. 1.89-fold in countries with ≤50 TB cases per 100,000 person-years), and geographical region (2.44-fold in Asia vs. 1.71-fold in Europe and 1.73-fold in the United States/Canada). The strength of the association was greater when TB diagnosis was confirmed microbiologically (3.03-fold) and when diabetes was identified through blood testing (3.10-fold) or in cases of uncontrolled diabetes (3.30-fold). Overall, diabetes was associated with a twofold to fourfold increased risk of active TB, with the association being more pronounced when based on biological testing rather than medical records or self-reports (
). Another systematic review of 30 studies found that the overall relative risk of developing active TB in patients with diabetes ranged from 1.16 to 7.83 compared to those without diabetes (
,
,
). In a systematic review and meta-analysis including more than 17,000 TB cases, diabetes was associated with an approximately threefold increased risk of TB (
). A fourth systematic review, conducted in accordance with the Meta-analysis Of Observational Studies in Epidemiology (MOOSE) guidelines, included a random-effects meta-analysis of 13 cohort studies (
). The pooled analysis demonstrated that diabetes was associated with an increased risk of TB, with a relative risk of 3.11 (95% CI 2.27–4.26). Notably, the relative risk varied by region. It was lower in North America (RR 1.46) compared with Central America (RR 6.00), Europe (RR 4.40), and Asia (RR 3.11). Meta-regression analysis was subsequently performed to assess whether geographic region modified the association between diabetes and TB risk. The reported p-values (p=0.006 for Central America, p=0.004 for Europe, and p=0.03 for Asia) represent the statistical significance of the regional differences—that is, they indicate that region acted as a significant effect modifier of the diabetes-TB association (
).
Clinically, diabetes, particularly when poorly controlled, is linked to a more severe and contagious TB infection compared to the general population. TB in individuals with diabetes (TB-DM) is more frequently associated with pulmonary TB, rather than extrapulmonary forms of the disease, when compared to other conditions that compromise the immune system. Extrapulmonary TB is still more common in TB-DM individuals compared to individuals with TB without diabetes. TB-DM is also characterized by an increased occurrence of lung cavitations, positive sputum smears at diagnosis, fever, cough, hemoptysis, and false-negative tuberculin skin test results compared with individuals with TB without diabetes. Diabetes may prolong the duration of smear and culture positivity at the end of the intensive phase of TB treatment (
).
Patients with diabetes are more likely to present with TB affecting the lower lungs (
) and are also more prone to developing multilobar disease and pleural effusion (
). Additionally, diabetes is associated with a higher risk of treatment complications, relapse, and mortality (
). The treatment for TB can exacerbate certain conditions in individuals with diabetes: hyperglycemia may worsen during acute infection, isoniazid can aggravate peripheral neuropathy, and rifampicin may reduce the effectiveness of sulfonylurea drugs. Mortality is also higher among individuals with both diabetes and TB. For instance, data from Maryland showed that among TB-infected individuals, those with diabetes were 6.5–6.7 times more likely to die compared to those without diabetes (
). A meta-analysis reported that diabetes increases the risk of treatment failure in TB patients (OR 1.65, 95% CI 1.12–2.44); additionally, TB-DM patients have 1.74 times higher odds of mortality compared to those with TB without diabetes (95% CI 1.21–2.51) (
).
The relationship between diabetes and drug-resistant TB, including multidrug-resistant TB (MDR-TB), remains unclear. While some studies suggest that individuals with diabetes respond to TB treatment and are not necessarily more likely to develop multidrug resistance (
,
), the relapse rate in patients with diabetes is four times greater than in those without diabetes (
). Contrarily, a systematic review of 30 studies worldwide found that TB-DM patients were 19% more likely to develop MDR-TB compared to TB patients without diabetes (HR <1, 95% CI 0.60–0.96, p<0.001) (
). Similarly, another analysis of 24 observational studies from 15 different countries revealed a significant positive association between diabetes and MDR-TB (OR 1.97, 95% CI 1.58–2.45, I2 38.2%, p-value for heterogeneity=0.031), irrespective of the country’s income level, the type of diabetes, the method of TB or diabetes diagnosis, or the design of the primary studies (
). Nevertheless, two independent studies by Ragouraman et al. (
) and Gautam et al. (
) in 2021 found no evidence of an increased risk of TB recurrence with drug-resistant strains among people with diabetes. This observation underscores the need for further research into the TB-DM population.
TB management in patients with diabetes presents unique challenges despite use of the same standard first-line regimen (isoniazid, rifampin, pyrazinamide, and ethambutol). Current WHO and American Thoracic Society (ATS)/CDC/IDSA guidelines emphasize close clinical and microbiologic follow-up and integrated management of both conditions to improve treatment success and reduce relapse (
,
).
Mechanisms by Which Diabetes Increases Susceptibility to Infection
Emphysematous Pyelonephritis
CKD is associated with impaired renal perfusion, reduced clearance of toxins, and impaired immune responses. These factors create an environment in which infections are more likely to progress rapidly and become severe. Chronic structural changes in the renal parenchyma, such as scarring, reduced vascularity, and tubular dysfunction, can limit local host defenses and reduce the effective delivery of antibiotics to infected tissue. Hypertension contributes by accelerating vascular injury and ischemia in renal tissue; it also compounds diabetes-related microvascular damage and diminishes the kidney’s ability to mount an adequate inflammatory or perfusion response. Together, CKD and hypertension increase susceptibility to infection, impair infection clearance, and are associated with more severe presentations and worse outcomes in EPN.
Skin and Soft Tissue Infections
Persistent hyperglycemia induces mitochondrial dysfunction and enhances the production of reactive oxygen species, which subsequently leads to oxidative stress. Chronic oxidative stress at the cellular level interferes with insulin signaling pathways and amplifies inflammatory responses. Prolonged exposure to hyperglycemia, coupled with oxidative stress, free radical accumulation, and sustained inflammation, contributes to end-organ damage. Furthermore, compromised skin barrier integrity, suboptimal vascularization, and diabetic neuropathy collectively exacerbate the risk of bacterial invasion in patients with diabetes (
).
Fungal Skin and Soft Tissue Infections
In patients with poorly controlled diabetes, elevated glucose levels in vaginal secretions provide a nutrient-rich environment conducive to the growth of Candida. Additionally, hyperglycemia disrupts normal vaginal microbiota and alters local pH, further enhancing Candida spp. virulence (
). The initial adhesion of Candida to vaginal epithelial cells is critical for colonization and the establishment of infection (
).
Necrotizing (Malignant) Otitis Externa
The increased risk of NOE in patients with diabetes is primarily thought to be driven by underlying diabetic macroangiopathy and microangiopathy, which disrupt tissue perfusion and cause immunologic and healing dysfunction by preventing chemotaxis of white blood cells. Additionally, the higher pH of cerumen in patients with diabetes creates a more favorable environment for pathogenic growth (
,
).
Group B Streptococcus Infections
In patients with diabetes, hyperglycemia causes altered immune function, which affects leukocyte function and increases proinflammatory cytokines. This results in impaired chemotaxis, phagocytosis, opsonization, and pathogen response. Peripheral vascular disease and diabetic neuropathy further exacerbate infection risks and poor outcomes by causing sensory loss and impairing wound healing and immune cell migration (
,
). Consequently, patients with diabetes are at higher risk for GBS and other common and atypical infections.
Tuberculosis
Numerous studies in both animal models and human subjects have explored the potential biological mechanisms underlying the causal association between diabetes and the increased risk of TB. Current data indicate that individuals with diabetes exhibit a higher bacterial load and reduced T helper 1 cell adaptive immunity, characterized by lower production of interferon-γ, interleukin-12, and nitric oxide (
,
). Additionally, monocytes from individuals with diabetes demonstrate impaired chemotaxis, while alveolar macrophages show decreased hydrogen peroxide production, resulting in reduced oxidative killing potential and diminished phagocytosis (
,
). Furthermore, vitamin D deficiency, which impairs immunity against Mycobacterium tuberculosis in mice (
), is also prevalent in human TB patients (
). These findings suggest a causal relationship between diabetes and TB, with hyperglycemia and its impact on physical barriers and immune function playing a significant role (
).
There is also the question of whether TB can lead to hyperglycemia and diabetes. TB patients have higher rates of impaired glucose tolerance compared to community controls (
). Metabolic decompensation due to infection and infection-induced insulin resistance can result in transient hyperglycemia (
,
). However, it remains unclear whether persistent impaired glucose tolerance and diabetes are directly caused by TB or if these conditions are simply newly diagnosed during TB treatment (
).
Implementing Evidence-Based Care for Infections Associated With Diabetes
The adoption of evidence-based care for diabetes-related infections relies on well-established implementation strategies. Implementation strategies are approaches that address barriers, improve efficiency, and ensure long-term sustainability of an adopted evidence-based intervention or treatment plan (
). Key strategies include comprehensive infection prevention measures, patient education and empowerment, multidisciplinary collaboration, and promoting continuous quality improvement.
Comprehensive Infection Prevention Strategies
Preventing diabetes-related infections requires a multifaceted approach incorporating strict infection control measures, antimicrobial stewardship, glycemic control, and early detection of complications. In healthcare settings, rigorous hand hygiene protocols, appropriate use of personal protective equipment, and environmental cleaning are essential for minimizing pathogen transmission. Antibiotic stewardship programs help preserve the effectiveness of existing antibiotics, improve patient outcomes, and reduce the spread of resistant bacteria (
).
Optimizing glycemic control is another important strategy. A study examining infection risk and glycemic control found that fasting plasma glucose levels above 200 mg/dL (>11.1 mmol/L) were associated with increased infection-related morbidity and mortality, particularly in older adults with a higher baseline infection risk (
). A review that assessed the effects of intensive insulin therapy with tight glycemic control versus conventional control on infection risk and neurological outcomes in critically ill neurosurgical and neurological patients showed that maintaining target blood glucose levels reduces infection risk and improves neurological outcome (
).
Additional infection prevention measures should be integrated directly into diabetes care. These include: (a) timely and appropriate antibiotic therapy to ensure effective treatment while minimizing resistance; (b) proactive vaccination against influenza and pneumococcal disease, which should be routinely reviewed and administered within diabetes clinics, rather than deferred solely to primary care, to protect at-risk individuals; and (c) early detection and management of foot ulcers, coupled with proper wound care, to prevent complications and reduce the risk of amputations.
Patient Education and Empowerment
Educating and empowering individuals with diabetes is important for reducing infection risks and improving health outcomes. Effective strategies include raising awareness about infection susceptibility, educating on prevention techniques including vaccinations against influenza and pneumococcal disease, encouraging medication adherence, and supporting regular self-care behaviors, particularly blood glucose monitoring, eating a healthy diet, engaging in regular physical activity, and monitoring feet for cuts, abrasions, or irritations that could lead to infections. These efforts, aside from improving glycemic control, enhance self-management which can help reduce the frequency of infection episodes, prevent secondary complications and decrease the likelihood of emergency room visits and hospitalizations (
). Existing patient education, including strategies and content for Diabetes Self-Management Education and Support (DSMES), could consider an emphasis on infections and risk for infections to maximize prevention using existing models of education.
Multidisciplinary Team Collaboration
Implementing evidence-based guidelines helps ensure consistency in infection prevention and management, while ongoing training and education keep healthcare providers informed about the latest research and best practices. This integrated approach strengthens proactive infection management and supports personalized diabetes care. Evidence from a systematic review shows that team-based care reduced major amputations in 94% of studies by consistently addressing glycemic control, local wound management, vascular disease, and infection in a timely and coordinated manner among patients with diabetic foot ulcerations (
). Collaboration among physicians, nurses, pharmacists, dietitians, and podiatrists ensures comprehensive, individualized care supported by effective communication and standardized protocols.
Continuous Quality Improvement
Ensuring that diabetes-related infection care remains effective requires a commitment to continuous quality improvement. Regularly reviewing and updating care protocols based on emerging research and best practices enhance patient outcomes. Monitoring vaccine protocols, infection rates, and other key indicators helps identify trends and areas needing intervention, while audits and feedback sessions enable healthcare teams to evaluate existing strategies and refine them for better results. Fostering a culture of continuous learning promotes collaboration, innovation, and accountability among providers.
To achieve these improvements, the American Diabetes Association recommends aligning diabetes management approaches with the Chronic Care Model (CCM) (
). A 5-year study evaluating effectiveness of CCM in 53,436 individuals with type 2 diabetes in primary care settings found that its implementation significantly reduced the incidence of diabetes-related complications and all-cause mortality (
). Despite various interventions, fragmented healthcare systems, limited clinical information capabilities, service duplication, and poor care coordination continue to hinder optimal diabetes care. The CCM provides a structured framework for improving the prevention and management of diabetes-related infections through six core elements (
):
• Delivery system design – shifting from reactive to proactive, team-based care for coordinated prevention through routine infection risk screening, vaccination review, and early wound care.
• Self-management support – empowering patients to actively participate in their footcare.
• Decision support – applying evidence-based decision tools at the point of care, such as vaccination protocols and antibiotic stewardship guidelines.
• Clinical information systems – utilizing clinical information systems, such as registries, for tracking vaccination status, antibiotic use, and foot examination completion.
• Community resources and policies – strengthening partnerships with local organizations to improve access to wound care, vaccination, infection screening, and diabetes education programs.
• Health systems – fostering a culture focused on quality improvement, which strengthens early detection and management of diabetes-related infections through routine performance monitoring, evidence-based practices, and feedback that enhance infection prevention and patient outcomes.
Conclusion
This article presents a broad overview of infections associated with diabetes by examining the prevalence of selected infections in persons with and without diabetes. Evidence shows that several infections and causative organisms are more prevalent in individuals diagnosed with diabetes, though no infection appears to occur exclusively in individuals with diabetes. From 1999 to 2023, individuals with diabetes in the United States experienced a higher burden of infections compared to those without diabetes. The adoption of implementation strategies, including patient education and empowerment, multidisciplinary collaboration, comprehensive infection prevention measures, and promoting continuous quality improvement will address barriers, improve efficiency, and ensure long-term sustainability of evidence-based intervention or treatment plans for infections associated with diabetes.
List of Abbreviations
ACIPAdvisory Committee on Immunization Practices
APNacute pyelonephritis
ASBasymptomatic bacteriuria
CAPcommunity-acquired pneumonia
CCMChronic Care Model
CDCCenters for Disease Control and Prevention
CDIClostridioides difficile infection
CIconfidence interval
CKDchronic kidney disease
COVID-19coronavirus disease of 2019
CRBSIcatheter-related bloodstream infection
cSSTIcomplicated skin and soft tissue infection
CTcomputed tomography
DKAdiabetic ketoacidosis
ECemphysematous cholecystitis
EPNemphysematous pyelonephritis
FDG-PETfluorodeoxyglucose positron emission tomography
GBSgroup B Streptococcus
HAIhospital-acquired infection
HCUPHealthcare Cost and Utilization Project
HRhazard ratio
ICD-9/10International Classification of Diseases, Ninth/Tenth Revision
ICUintensive care unit
IDSAInfectious Diseases Society of America
iGBSinvasive group B Streptococcus
IWGDFInternational Working Group on the Diabetic Foot
MDR-TBmultidrug-resistant tuberculosis
MRImagnetic resonance imaging
MRSAmethicillin-resistant Staphylococcus aureus
NAMCSNational Ambulatory Medical Care Survey
NFnecrotizing fasciitis
NOEnecrotizing otitis externa
NVSSNational Vital Statistics System
ORodds ratio
RRrelative risk
RSVrespiratory syncytial virus
SARS-CoV-2severe acute respiratory syndrome coronavirus 2
SGLT2 sodium-glucose cotransporter-2
SSTIskin and soft tissue infection
TBtuberculosis
TB-DMtuberculosis in individuals with diabetes mellitus
UTIurinary tract infection
WHOWorld Health Organization
WMDweighted mean difference
Conversion
Glucose: mg/dL x 0.0555 = mmol/L
Acknowledgment
This is an update of: Egede LE, Hull BJ, Williams JS: Infections Associated with Diabetes. Chapter 30 in Diabetes in America, 3rd ed. Cowie CC, Casagrande SS, Menke A, Cissell MA, Eberhardt MS, Meigs JB, Gregg EW, Knowler WC, Barrett-Connor E, Becker DJ, Brancati FL, Boyko EJ, Herman WH, Howard BV, Narayan KMV, Rewers M, Fradkin JE, Eds. Bethesda, MD, National Institutes of Health, NIH Pub No. 17-1468, 2018, p. 30.1–30.25.
Article History
Received in final form on December 2, 2025.
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175.176.Appendices
APPENDIX TABLE A1.
List of ICD-9 and ICD-10 Codes Used in This Article
INFECTIONICD-9 CODESICD-10 CODESRespiratory Tract InfectionsInfluenza480–488J10.1, J18.9Sinusitis and bronchitis461, 466J32.9, J40COVID-19NAU07.1, B97.2Urinary Tract InfectionsAsymptomatic bacteriuria791.9N39.0Cystitis595N30.9Pyelonephritis590.1, 590.8N10Perinephric abscess590.2N15.1Skin and Connective Tissue InfectionsOral and vaginal candidiasis112.0–112.3B37.0, B37.3Onychomycosis110.1B35.1Intertrigo and erythematous conditions695.89L26, L30.4, L53.8, L92.0, L95.1, L98.2Cellulitis and impetigo682, 684L03, L01Foot ulcers707.1L97Osteomyelitis730.2M86.9Necrotizing fasciitis728.86M72.6Gangrene785.4I96Hospital-Acquired InfectionsSepsis38A41.9Postoperative wound infections998.59T81.49Other Infections Associated With DiabetesNecrotizing otitis externa380.14H60.2Mucormycosis117.7B46.5Emphysematous cholecystitis575K81.0OtherTuberculosis010–018A15.9HIV042–044B20Diabetes250, 357.2, 362.0, 366.41, 648.0, 775.1E10–E14The transition from ICD-9 to ICD-10 coding occurred in late 2015. COVID-19, coronavirus disease of 2019; HIV, human immunodeficiency virus; ICD-9/10, International Classification of Diseases, Ninth/Tenth Revision; NA, not applicable.
SOURCE: Reference (
)
APPENDIX TABLE A2.
Percentage of Deaths Caused by Infections, by Diabetes Status and Infection Type, U.S., 1999–2023
YEARPERCENTDiabetesNo DiabetesAny Infection*Respiratory Tract InfectionsUrinary Tract InfectionsSkin And Connective Tissue InfectionsHospital-Acquired InfectionsOther Infections Associated With DiabetesHIVAny Infection*Respiratory Tract InfectionsUrinary Tract InfectionsSkin And Connective Tissue InfectionsHospital-Acquired InfectionsOther Infections Associated With DiabetesHIV19993.101.270.670.160.930.030.044.502.390.590.061.170.030.2720003.161.350.650.170.920.030.044.532.410.580.071.190.030.2620013.261.360.650.180.980.040.054.492.330.580.081.230.030.2520023.381.430.640.201.020.050.054.632.430.570.081.280.030.2520033.331.350.650.241.000.040.064.602.370.570.101.300.030.2320043.231.260.660.250.970.040.054.512.240.580.111.310.040.2320053.351.310.680.251.020.040.054.552.290.610.101.300.040.2120063.171.190.670.260.960.040.064.352.090.600.111.320.030.2020073.101.140.650.260.960.040.054.302.020.600.111.350.040.1820082.851.140.420.250.950.040.044.212.070.460.101.370.040.1720092.791.090.420.250.930.050.044.081.930.450.111.380.040.1620102.701.000.410.250.950.040.043.961.870.450.121.340.040.1320112.761.070.420.280.900.040.054.041.940.460.121.360.040.1220122.630.990.390.280.890.040.033.911.830.450.121.350.040.1120132.621.020.380.210.920.040.044.061.930.450.131.410.040.1020142.500.930.390.220.880.040.044.001.820.460.141.440.040.1020152.520.890.400.250.900.050.044.021.820.460.151.460.050.0920162.430.810.390.240.900.050.033.811.650.460.151.420.050.0920172.450.870.370.250.870.050.023.781.640.440.161.420.050.0720182.440.860.370.260.870.050.033.731.630.430.161.400.050.0720192.290.760.370.280.800.050.023.451.430.410.171.320.050.07202016.5715.250.320.240.690.040.0212.9211.100.390.161.170.050.06202116.7715.310.360.300.740.050.0214.5812.720.410.171.180.050.0520228.556.910.390.320.850.060.038.756.730.450.191.270.050.0520233.972.200.420.330.930.060.034.882.790.450.211.320.060.05Diabetes status and infections are defined based on International Classification of Diseases, Ninth and Tenth Revision codes (
). HIV, human immunodeficiency virus.
* Any infection among those listed in this table.
SOURCE: National Vital Statistics System 1999–2023
APPENDIX TABLE A3.
Age-Standardized Percentage of Hospital Discharges Listing Infection, by Diabetes Status and Infection Type, U.S., 1999–2021
TYPE OF INFECTIONPERCENT (STANDARD ERROR)19992000200120022003200420052006200720082009201020112012201320142015201620172018201920202021DiabetesAny infection (among those listed below)20.5 (0.16)19.7 (0.16)19.5 (0.16)19.9 (0.15)20.6 (0.16)20.6 (0.17)21.5 (0.19)21.3 (0.18)21.7 (0.16)22.3 (0.18)22.8 (0.17)22.5 (0.19)23.7 (0.19)23.6 (0.09)24.5 (0.10)25.3 (0.10)25.9 (0.11)28.2 (0.12)28.4 (0.12)28.8 (0.12)27.9 (0.12)34.1 (0.14)34.9 (0.15)Respiratory tract infectionsAny7.9 (0.08)7.2 (0.08)7.0 (0.08)7.2 (0.08)7.8 (0.09)7.5 (0.09)8.2 (0.09)7.8 (0.10)8.1 (0.09)8.6 (0.10)9.0 (0.10)8.2 (0.11)8.6 (0.10)8.4 (0.05)8.9 (0.06)8.8 (0.05)9.0 (0.06)6.7 (0.05)6.8 (0.05)6.6 (0.05)5.6 (0.05)13.7 (0.10)14.9 (0.04)Influenza6.7 (0.08)6.3 (0.08)6.1 (0.08)6.4 (0.07)6.9 (0.08)6.6 (0.08)7.3 (0.09)7.0 (0.09)7.2 (0.09)7.7 (0.09)8.0 (0.10)7.4 (0.10)7.8 (0.10)7.6 (0.05)8.1 (0.05)8.1 (0.05)8.3 (0.05)6.2 (0.05)6.3 (0.05)6.2 (0.05)5.2 (0.04)5.6 (0.05)4.7 (0.09)Sinusitis and bronchitis1.3 (0.03)1.0 (0.02)0.9 (0.02)0.9 (0.02)1.0 (0.03)1.0 (0.02)1.0 (0.02)0.9 (0.03)0.9 (0.02)1.1 (0.03)1.1 (0.03)0.9 (0.02)0.9 (0.02)0.9 (0.01)0.9 (0.01)0.8 (0.01)0.9 (0.02)0.6 (0.01)0.6 (0.01)0.5 (0.01)0.5 (0.01)0.3 (0.01)0.2 (0.01)COVID-190.1 (0.00)7.9 (0.08)10.1 (0.07)Urinary tract infectionsAny0.9 (0.02)0.9 (0.02)0.9 (0.02)0.9 (0.02)0.9 (0.02)0.9 (0.02)1.0 (0.02)1.0 (0.02)1.0 (0.02)1.0 (0.03)1.1 (0.03)1.2 (0.03)1.3 (0.03)1.4 (0.02)1.4 (0.02)1.5 (0.02)1.7 (0.02)9.8 (0.06)9.3 (0.06)9.0 (0.07)8.4 (0.06)8.2 (0.06)8.1 (0.06)Asymptomatic bacteriuria0.0 (0.00)0.0 (0.00)0.0 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.01)0.1 (0.00)0.1 (0.00)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)9.0 (0.06)8.4 (0.06)8.2 (0.06)7.6 (0.06)7.4 (0.06)7.3 (0.06)Cystitis0.1 (0.00)0.1 (0.00)0.1 (0.01)0.1 (0.00)0.1 (0.00)0.1 (0.01)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.3 (0.01)Pyelonephritis0.8 (0.02)0.7 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.9 (0.02)0.9 (0.02)0.9 (0.02)1.0 (0.02)1.1 (0.03)1.1 (0.02)1.1 (0.02)1.2 (0.02)1.3 (0.02)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)Perinephric abscess0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)Skin and connective tissue infectionsAny9.6 (0.10)9.5 (0.10)9.7 (0.11)9.8 (0.11)10.0 (0.10)10.2 (0.10)10.4 (0.12)10.6 (0.11)10.7 (0.10)10.6 (0.11)10.7 (0.09)11.0 (0.10)11.5 (0.12)11.4 (0.06)11.7 (0.06)12.1 (0.06)12.2 (0.07)10.5 (0.06)10.6 (0.06)11.2 (0.06)11.4 (0.07)10.8 (0.06)10.7 (0.06)Oral and vaginal candidiasis1.2 (0.03)1.1 (0.02)1.2 (0.03)1.2 (0.03)1.2 (0.03)1.2 (0.03)1.3 (0.03)1.2 (0.03)1.3 (0.03)1.4 (0.03)1.5 (0.03)1.5 (0.03)1.5 (0.03)1.6 (0.02)1.5 (0.02)1.6 (0.02)1.5 (0.02)0.8 (0.01)0.8 (0.01)0.8 (0.01)0.8 (0.01)0.8 (0.01)0.7 (0.01)Onychomycosis0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.1 (0.01)0.2 (0.01)Intertrigo and erythematous conditions0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.1 (0.00)0.1 (0.00)0.0 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)Cellulitis and impetigo5.2 (0.06)5.4 (0.07)5.4 (0.07)5.6 (0.08)5.7 (0.07)6.0 (0.07)6.3 (0.09)6.3 (0.08)6.5 (0.07)6.4 (0.08)6.4 (0.07)6.6 (0.08)6.9 (0.09)7.0 (0.05)7.1 (0.05)7.3 (0.05)7.4 (0.05)6.9 (0.05)7.0 (0.05)7.1 (0.06)7.3 (0.06)6.8 (0.05)6.7 (0.05)Foot ulcers3.3 (0.06)3.3 (0.06)3.6 (0.07)3.5 (0.06)3.5 (0.06)3.6 (0.06)3.5 (0.06)3.7 (0.06)3.6 (0.06)3.5 (0.05)3.4 (0.05)3.5 (0.06)3.8 (0.06)3.7 (0.04)4.0 (0.04)4.2 (0.04)4.3 (0.04)3.9 (0.04)4.1 (0.04)4.4 (0.04)4.7 (0.04)4.4 (0.04)4.4 (0.04)Osteomyelitis0.8 (0.02)0.8 (0.03)0.8 (0.02)0.8 (0.03)0.9 (0.02)0.9 (0.02)0.9 (0.03)1.0 (0.03)1.1 (0.03)1.2 (0.03)1.3 (0.03)1.3 (0.03)1.5 (0.04)1.4 (0.02)1.6 (0.02)1.7 (0.02)1.7 (0.02)0.8 (0.01)0.8 (0.01)0.9 (0.02)1.0 (0.02)1.0 (0.02)1.0 (0.02)Necrotizing fasciitis0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.3 (0.01)0.3 (0.01)Fournier’s gangrene1.1 (0.03)1.0 (0.03)1.0 (0.03)0.9 (0.02)0.9 (0.03)0.9 (0.03)0.8 (0.02)0.8 (0.02)0.7 (0.02)0.7 (0.02)0.7 (0.02)0.7 (0.02)0.7 (0.02)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.8 (0.01)0.2 (0.01)0.2 (0.01)0.8 (0.01)0.8 (0.02)0.8 (0.02)0.8 (0.01)Hospital-acquired infectionsAny3.8 (0.06)3.5 (0.06)3.5 (0.06)3.6 (0.07)3.7 (0.07)3.8 (0.08)3.8 (0.09)4.1 (0.09)4.4 (0.08)4.7 (0.09)4.9 (0.09)5.1 (0.10)5.7 (0.12)6.0 (0.05)6.8 (0.06)7.6 (0.07)8.5 (0.07)7.1 (0.07)7.8 (0.07)8.2 (0.07)8.3 (0.08)8.3 (0.07)8.1 (0.07)Sepsis3.0 (0.06)2.8 (0.06)2.8 (0.06)2.8 (0.07)2.9 (0.07)3.0 (0.08)3.0 (0.09)3.3 (0.09)3.6 (0.08)3.9 (0.10)4.2 (0.09)4.4 (0.10)5.0 (0.12)5.4 (0.05)6.2 (0.06)7.0 (0.07)7.9 (0.07)6.5 (0.07)7.2 (0.07)7.6 (0.08)7.7 (0.08)7.7 (0.07)7.5 (0.07)Postoperative wound infections0.8 (0.03)0.8 (0.02)0.8 (0.02)0.9 (0.02)0.9 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)Other infections associated with diabetesAny0.1 (0.00)0.1 (0.01)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.2 (0.00)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.01)0.2 (0.00)Necrotizing otitis externa0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)Mucormycosis0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)Emphysematous cholecystitis0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.2 (0.01)0.2 (0.01)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.01)0.2 (0.01)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)OtherTuberculosis0.1 (0.01)0.1 (0.01)0.1 (0.00)0.1 (0.01)0.1 (0.00)0.1 (0.00)0.1 (0.01)0.1 (0.01)0.0 (0.00)0.0 (0.00)0.1 (0.01)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)HIV0.5 (0.05)0.5 (0.04)0.4 (0.04)0.4 (0.03)0.4 (0.03)0.4 (0.04)0.4 (0.03)0.5 (0.04)0.4 (0.03)0.4 (0.03)0.4 (0.03)0.4 (0.04)0.3 (0.03)0.3 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)No DiabetesAny infection (among those listed below)13.2 (0.14)12.4 (0.13)12.2 (0.13)12.8 (0.13)13.5 (0.13)13.6 (0.14)14.6 (0.15)14.3 (0.14)14.5 (0.14)15.2 (0.14)15.6 (0.14)15.7 (0.15)16.0 (0.14)16.0 (0.07)16.6 (0.07)17.0 (0.08)12.1 (0.06)19.1 (0.08)18.9 (0.08)18.9 (0.09)18.1 (0.08)22.1 (0.10)23.4 (0.10)Respiratory tract infectionsAny7.8 (0.09)7.1 (0.09)6.7 (0.09)7.1 (0.09)7.6 (0.10)7.4 (0.09)8.0 (0.10)7.6 (0.09)7.7 (0.10)8.2 (0.10)8.4 (0.11)8.1 (0.11)8.3 (0.10)8.1 (0.05)8.5 (0.05)8.4 (0.05)6.0 (0.04)6.0 (0.04)6.1 (0.04)5.9 (0.04)5.1 (0.04)10.0 (0.07)11.4 (0.07)Influenza6.6 (0.08)6.2 (0.07)5.8 (0.08)6.2 (0.08)6.6 (0.08)6.4 (0.08)7.1 (0.09)6.7 (0.08)6.9 (0.09)7.3 (0.09)7.5 (0.09)7.2 (0.09)7.5 (0.09)7.3 (0.04)7.7 (0.05)7.7 (0.05)5.4 (0.03)5.6 (0.04)5.6 (0.04)5.5 (0.04)4.6 (0.04)5.0 (0.04)4.3 (0.03)Sinusitis and bronchitis1.3 (0.03)1.0 (0.03)1.0 (0.03)1.0 (0.03)1.1 (0.03)1.1 (0.03)1.1 (0.04)1.0 (0.03)1.0 (0.03)1.1 (0.04)1.1 (0.03)1.0 (0.04)1.0 (0.03)1.0 (0.02)1.0 (0.02)0.9 (0.02)0.7 (0.02)0.5 (0.01)0.5 (0.01)0.5 (0.01)0.4 (0.01)0.3 (0.01)0.2 (0.01)COVID-190.1 (0.00)4.8 (0.05)6.9 (0.05)Urinary tract infectionsAny0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.8 (0.01)0.9 (0.02)0.9 (0.02)0.9 (0.01)1.0 (0.01)1.0 (0.01)0.8 (0.01)7.5 (0.04)7.0 (0.05)6.8 (0.05)6.4 (0.04)6.4 (0.04)6.4 (0.04)Asymptomatic bacteriuria0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)7.0 (0.04)6.5 (0.04)6.3 (0.04)5.9 (0.04)5.9 (0.04)5.9 (0.04)Cystitis0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.1 (0.00)0.1 (0.01)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)Pyelonephritis0.5 (0.01)0.5 (0.01)0.5 (0.01)0.5 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.8 (0.01)0.6 (0.01)0.4 (0.00)0.4 (0.01)0.4 (0.01)0.4 (0.00)0.3 (0.00)0.3 (0.00)Perinephric abscess0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)Skin and connective tissue infectionsAny3.1 (0.04)3.1 (0.04)3.2 (0.04)3.4 (0.04)3.6 (0.04)3.8 (0.05)4.1 (0.05)4.2 (0.05)4.3 (0.05)4.5 (0.05)4.6 (0.04)4.8 (0.05)4.8 (0.05)4.8 (0.02)4.8 (0.02)4.9 (0.02)3.4 (0.02)4.2 (0.02)4.1 (0.02)4.2 (0.02)4.2 (0.02)4.0 (0.02)4.1 (0.02)Oral and vaginal candidiasis0.7 (0.02)0.6 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.8 (0.02)0.8 (0.02)0.8 (0.02)0.9 (0.02)1.0 (0.02)1.0 (0.02)1.1 (0.02)1.1 (0.02)1.0 (0.01)1.0 (0.01)1.0 (0.01)0.7 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.5 (0.01)0.5 (0.01)Onychomycosis0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.01)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)Intertrigo and erythematous conditions0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)Cellulitis and impetigo1.8 (0.03)1.9 (0.03)2.0 (0.03)2.1 (0.03)2.3 (0.03)2.4 (0.03)2.6 (0.03)2.7 (0.03)2.7 (0.03)2.8 (0.03)2.9 (0.03)3.0 (0.04)3.0 (0.04)3.0 (0.02)3.1 (0.02)3.1 (0.02)2.2 (0.01)2.9 (0.02)2.9 (0.02)3.0 (0.02)2.9 (0.02)2.8 (0.02)2.8 (0.02)Foot ulcers0.4 (0.01)0.4 (0.01)0.5 (0.01)0.5 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.5 (0.00)0.7 (0.01)0.6 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)0.7 (0.01)Osteomyelitis0.1 (0.00)0.1 (0.00)0.1 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.01)0.2 (0.01)0.2 (0.00)0.2 (0.01)0.2 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.00)0.3 (0.00)0.3 (0.00)0.2 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)Necrotizing fasciitis0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.1 (0.00)0.1 (0.00)Fournier’s gangrene0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)Hospital-acquired infectionsAny2.6 (0.04)2.5 (0.04)2.6 (0.04)2.7 (0.04)2.8 (0.04)3.0 (0.04)3.2 (0.05)3.3 (0.06)3.6 (0.06)3.9 (0.07)4.0 (0.06)4.3 (0.07)4.6 (0.08)4.8 (0.04)5.3 (0.04)6.0 (0.05)4.5 (0.03)5.4 (0.04)5.8 (0.05)6.0 (0.05)6.1 (0.05)6.3 (0.05)6.2 (0.05)Sepsis2.1 (0.04)2.0 (0.04)2.0 (0.04)2.1 (0.04)2.3 (0.04)2.4 (0.05)2.6 (0.05)2.8 (0.06)3.0 (0.06)3.3 (0.07)3.4 (0.06)3.7 (0.07)4.0 (0.08)4.3 (0.04)4.8 (0.04)5.6 (0.05)4.2 (0.03)5.0 (0.04)5.3 (0.05)5.6 (0.05)5.6 (0.05)5.8 (0.05)5.7 (0.05)Postoperative wound infections0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.7 (0.01)0.7 (0.02)0.7 (0.02)0.7 (0.02)0.7 (0.02)0.6 (0.01)0.6 (0.01)0.6 (0.01)0.4 (0.00)0.5 (0.01)0.5 (0.01)0.6 (0.01)0.6 (0.01)0.5 (0.01)0.6 (0.01)Other infections associated with diabetesAny0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.1 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)Necrotizing otitis externa0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)Mucormycosis0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)Emphysematous cholecystitis0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.1 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)0.2 (0.00)OtherTuberculosis0.1 (0.01)0.1 (0.00)0.1 (0.00)0.1 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.0 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)0.01 (0.00)HIV0.5 (0.05)0.5 (0.04)0.4 (0.04)0.4 (0.04)0.4 (0.03)0.5 (0.04)0.4 (0.04)0.5 (0.04)0.4 (0.03)0.4 (0.03)0.4 (0.04)0.4 (0.04)0.4 (0.03)0.4 (0.01)0.4 (0.01)0.3 (0.01)0.2 (0.01)0.4 (0.01)0.4 (0.01)0.4 (0.01)0.3 (0.01)0.3 (0.01)0.3 (0.01)Diabetes status and infections are defined based on International Classification of Diseases, Ninth and Tenth Revision codes (
). Data are age standardized to the HCUP 2020 National (Nationwide) Inpatient Sample (NIS), using age groups 0–44, 45–64, and ≥65 years. COVID-19, coronavirus disease of 2019; HIV, human immunodeficiency virus.
1Estimates are 0.0 (0.00) due to rounding; estimates are <0.05 (<0.005).
SOURCE: Healthcare Cost and Utilization Project (HCUP) 1999–2021
APPENDIX TABLE A4.
Age-Standardized Percentage of Outpatient Visits Listing Any Infection, by Diabetes Status, U.S., 1999–2022
SURVEY YEARDIABETESNO DIABETESWeighted NPercent (SE)Weighted NPercent (SE)Physician Office Visits199934,067,3083.4 (0.72)715,567,7253.4 (0.35)200039,447,7622.7 (0.56)771,777,3903.0 (0.29)200142,808,7592.9 (1.08)1836,435,4932.6 (0.25)200244,619,7572.7 (1.03)1843,325,9572.9 (0.22)200343,602,5625.1 (1.49)858,213,0213.0 (0.34)200445,595,6285.0 (1.59)1862,995,6863.0 (0.24)200544,720,8985.1 (2.10)2906,914,4413.1 (0.22)200640,056,6003.9 (1.51)1847,575,5903.0 (0.22)200744,497,4903.1 (0.99)1922,326,4112.6 (0.19)200846,389,4172.8 (1.12)2887,505,6343.3 (0.29)200957,316,1211.5 (0.55)1949,356,6613.4 (0.25)201049,947,9802.6 (0.55)938,409,8523.5 (0.28)201151,906,6611.0 (0.33)1909,608,8113.4 (0.26)201243,731,7413.5 (0.86)884,898,2123.5 (0.15)201351,122,7452.1 (0.56)871,473,7003.7 (0.20)201455,471,0182.6 (0.70)829,236,1523.4 (0.20)201569,316,3883921,492,0983.1 (0.35)201644,489,6581.9 (0.63)1839,235,4682.9 (0.26)201852,522,6241.5 (0.65)2807,863,0152.5 (0.40)201966,337,7561.5 (0.64)2970,146,6002.5 (0.35)Community Health Center Visits1999334,97325.2 (12.56)26,763,8483.2 (1.02)12000440,694311,876,1534.0 (1.45)1200159,55331,182,86432002224,04031,810,73732003178,73234,028,4412.3 (1.08)22004323,28531,942,5618.0 (3.32)22005580,102311,401,958320061,243,2573.8 (1.84)213,078,7785.2 (1.54)20072,153,2646.9 (2.96)225,344,0852.9 (0.65)20081,905,7582.4 (0.99)220,168,0093.3 (0.79)20093,774,130327,349,5744.8 (1.03)20102,061,392318,382,7813.9 (0.50)20112,644,9603.1 (1.16)122,868,4006.6 (1.35)20125,993,7374.5 (0.87)59,338,9855.7 (0.51)20134,769,5473.3 (0.63)48,834,8895.6 (0.50)20146,294,5853.7 (0.68)52,233,4114.9 (0.31)20155,681,3514.1 (1.03)45,629,0735.1 (0.32)202231,740,6704.2 (0.57)337,399,9343.1 (0.28)Diabetes status and infections are defined based on International Classification of Diseases, Ninth and Tenth Revision codes (
). Data are age-standardized to the NAMCS 1999–2016, 2018–2019, 2022, using age groups 0–44, 45–64, and ≥65 years. SE, standard error.
1Relative standard error >30%–40%
2Relative standard error >40%–50%
3Estimate is too unreliable to present; ≤1 case or relative standard error >50%.
SOURCE: National Ambulatory Medical Care Surveys (NAMCS) 1999–2022
All authors reported no conflicts of interest.